subject:(insulin)

University of Hawaii – Manoa

1. Greineisen, William Ernest. Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells.

Degree: 2016, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/101908

►

Ph.D. University of Hawaii at Manoa 2013.

This thesis presents evidence that mast cells (MC) chronically exposed to insulin respond by developing steatotic levels of… (more)

Subjects/Keywords: insulin

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APA (6^th Edition):

Greineisen, W. E. (2016). Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/101908

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Greineisen, William Ernest. “Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells.” 2016. Thesis, University of Hawaii – Manoa. Accessed February 19, 2020. http://hdl.handle.net/10125/101908.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Greineisen, William Ernest. “Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells.” 2016. Web. 19 Feb 2020.

Vancouver:

Greineisen WE. Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells. [Internet] [Thesis]. University of Hawaii – Manoa; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10125/101908.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Greineisen WE. Chronic exposure to an insulin-containing lipogenic stimulus results in ectopic cytoplasmic lipid accumulation and altered pro-inflammatory function in mast cells. [Thesis]. University of Hawaii – Manoa; 2016. Available from: http://hdl.handle.net/10125/101908

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New South Wales

2. Tang, Alice. Insulin-Sensitive Obesity: Prospective and Interventional Studies.

Degree: Clinical School - St Vincent's Hospital, 2017, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true

► BACKGROUND: Individuals with metabolically healthy/insulin-sensitive obesity (MHO/Obsen) have been shown to have a comparable metabolic profile to lean individuals. However, longitudinal change in metabolic parameters… (more)

▼ BACKGROUND: Individuals with metabolically healthy/insulin-sensitive obesity (MHO/Obsen) have been shown to have a comparable metabolic profile to lean individuals. However, longitudinal change in metabolic parameters in those with MHO/Obsen has not been comprehensively delineated with the gold-standard measure of insulin-sensitivity, the hyperinsulinaemic-euglycaemic clamp. The response of MHO/ Obsen cohorts to weight loss is also unclear. This study investigates the metabolic changes in the Obsen phenotype over time and in response to weight loss. METHODS: A cohort of 124 individuals was carefully phenotyped 6 years ago and categorised into lean, overweight/obese insulin-sensitive (Obsen) or resistant (Obres, using gender based median insulin-sensitivity cut-offs) and type 2 diabetes mellitus (T2DM). Sixty-nine participants were followed up in this study. A subcohort (n = 13) also underwent a 16-week caloric restriction intervention. A comprehensive assessment of metabolic health, including insulin sensitivity (using hyperinsulinaemic-euglcyaemic clamp), body fat composition, serum/plasma metabolic markers, energy metabolism and lifestyle parameters, was performed.RESULTS: There was an increase in total body fat, visceral adipose tissue mass, blood pressure and adipose tissue insulin resistance and a decrease in resting metabolic rate in the whole cohort over 6 years. Insulin sensitivity appeared to decrease over time in Obsen compared to the other groups. Physical activity increased and sugar intake decreased in Obres and T2DM. Saturated fat and trans-fat intake increased in the Obsen group. Insulin sensitivity in the 6 years prior to weight loss was inversely correlated to the change in insulin sensitivity induced by weight loss. Insulin sensitivity immediately prior to weight loss was inversely correlated to the change in resting metabolic rate induced by weight loss.CONCLUSION: Obsen is not an enduring phenotype over 6 years. Hence, clinical intervention should target all individuals with overweight/obesity, irrespective of apparent metabolic health. However, further investigation into the role that insulin sensitivity plays in the response to weight loss is required to ensure optimum management in Obsen individuals. Advisors/Committee Members: Greenfield, Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Samocha-Bonet, Dorit, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: Insulin resistance; Obesity; Insulin sensitivity

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APA (6^th Edition):

Tang, A. (2017). Insulin-Sensitive Obesity: Prospective and Interventional Studies. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Tang, Alice. “Insulin-Sensitive Obesity: Prospective and Interventional Studies.” 2017. Doctoral Dissertation, University of New South Wales. Accessed February 19, 2020. http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Tang, Alice. “Insulin-Sensitive Obesity: Prospective and Interventional Studies.” 2017. Web. 19 Feb 2020.

Vancouver:

Tang A. Insulin-Sensitive Obesity: Prospective and Interventional Studies. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2020 Feb 19]. Available from: http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true.

Council of Science Editors:

Tang A. Insulin-Sensitive Obesity: Prospective and Interventional Studies. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true

3. Bikman, Benjamin Thomas. Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle.

Degree: 2011, NC Docks

URL: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

► Activation of the insulin receptor substrate (IRS)-1 is necessary for proper transduction of the insulin signal. IRS-1 serine312(human)/307(rodent) phosphorylation however results in disruption of this… (more)

▼ Activation of the insulin receptor substrate (IRS)-1 is necessary for proper transduction of the insulin signal. IRS-1 serine312(human)/307(rodent) phosphorylation however results in disruption of this signal and subsequent insulin resistance. Inflammatory mediators such as the inhibitor of kappaB kinase beta; (IKK-beta) interrupt insulin signaling within insulin-sensitive tissues such as skeletal muscle. In contrast AMP-activated protein kinase (AMPK) a key metabolic enzyme increases insulin sensitivity. To study the association of IKK-beta and AMPK muscle biopsies were taken from post-bypass patients and control subjects. Post-bypass patients displayed similar levels of IKK-beta action and IRS1-pSer312 as the lean subjects and reduced levels compared with weight-matched control and morbidly obese subjects which supports evidence that IKK-beta phosphorylates IRS-1 Ser312 and reduces the insulin signal resulting in reduced whole-body insulin sensitivity. However these findings did not correlate with baseline differences in AMPK phosphorylation. To explore the role of AMPK in attenuating IKK-beta activity and ameliorating insulin resistance lean and obese Zucker rats were treated with metformin an AMPK activator. Despite no differences at baseline AMPK action was increased with metformin treatment in a fiber-type specific (white muscle) manner with a reduction in IKK-beta activity and IRS1-pSer307 in the muscle of obese rats only. To explore this relationship further myotubes from lean and morbidly obese humans were exposed to the saturated fatty acid palmitate in the presence or absence of AICAR to activate AMPK. In contrast to the lean obese myotubes demonstrated no depression in insulin signaling with lipid exposure. Co-incubation with AICAR prevented the lipid-induced decay of the insulin signal in the lean and improved the signal in the obese. AICAR-stimulated AMPK activation for the final 4 h of lipid exposure was not sufficient to restore phosphorylation of AS160. These data support the hypothesis that lipids induce insulin resistance via lipid-sensitive serine kinases that attenuate insulin signaling. Whereas AMPK activity does not appear to play a role in baseline differences of IKK-beta action and insulin signaling we present findings that the lipid-induced decay in the insulin signal can be prevented by acute activation of AMPK. These results provide valuable information explaining differences in skeletal muscle function in the lean and obese as well as elucidating a potential mechanism for insulin-sensitizing AMPK-activating agents.

Subjects/Keywords: Insulin resistance; Insulin – Receptors

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APA (6^th Edition):

Bikman, B. T. (2011). Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle. (Thesis). NC Docks. Retrieved from http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bikman, Benjamin Thomas. “Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle.” 2011. Thesis, NC Docks. Accessed February 19, 2020. http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bikman, Benjamin Thomas. “Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle.” 2011. Web. 19 Feb 2020.

Vancouver:

Bikman BT. Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle. [Internet] [Thesis]. NC Docks; 2011. [cited 2020 Feb 19]. Available from: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bikman BT. Modulation of IKKÎ² with AMPK Improves Insulin Sensitivity in Skeletal Muscle. [Thesis]. NC Docks; 2011. Available from: http://libres.uncg.edu/ir/ecu/f/0000-embargo-holder.txt

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Utah

4. Tidwell, Timothy James. Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet.

Degree: Honors BS;, Biology;, 2009, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1658/rec/651

► INTRODUCTION: People with diabetes are at high risk for cardiovascular disease; which is the major cause of death in diabetics. Current research suggests that excessive… (more)

▼ INTRODUCTION: People with diabetes are at high risk for cardiovascular disease; which is the major cause of death in diabetics. Current research suggests that excessive mitochondrial uncoupling is a potential mechanism for cardiac dysfunction in diabetic patients. Uncoupling protein 3 (UCP3) is an inner mitochondrial membrane protein that reduces the amount of reactive oxygen species (ROS) produced in the mitochondrial matrix by uncoupling the mitochondria. Mice lacking UCP3 (UCP3KO) have been shown to accumulate ROS and diacylglycerol in cardiac muscle. These two molecules have been shown to induce insulin resistance in skeletal muscle. The goal of my project was to determine if the absence of UCP3 in the heart will exacerbate diet-induced insulin resistance in the murine heart. MATERIALS AND METHODS: Whole heart homogenates were extracted from four groups of mice: (1) wild type (WT) fed normal chow (NC); (2) WT fed a high fat diet for 10 weeks (HF); (3) UCP3KO NC and (4) UCP3KO HF. Insulin signaling was examined using western-blotting to assess the phosphorylation status of key components of the insulin signaling pathway under non insulin and insulin-stimulated conditions in each group. Values form each group were analyzed using an ANOVA followed by a t test to determine any statistical significant differences between the groups. RESULTS: Phosphorylation of protein kinase B (Akt) (at serine 473 or threonine 308) and the downstream target glycogen synthase kinase 3 p at serine 9 was the same between all the groups. CONCLUSIONS: two major conclusions arise from this work; ( 1 ) 1 0 weeks of high fat diet does not affect insulin signaling in the heart and (2) despite increased ROS and DAG levels in the hearts of UCP3KO mice, insulin sensitivity was maintained. We speculate that UCP3KO mice have developed compensatory mechanisms that prevented the development of insulin resistance despite accumulation of compounds known to induce insulin resistance. These mechanisms remain to be determined in future studies.

Subjects/Keywords: Insulin resistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tidwell, T. J. (2009). Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1658/rec/651

Chicago Manual of Style (16^th Edition):

Tidwell, Timothy James. “Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet.” 2009. Masters Thesis, University of Utah. Accessed February 19, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1658/rec/651.

MLA Handbook (7^th Edition):

Tidwell, Timothy James. “Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet.” 2009. Web. 19 Feb 2020.

Vancouver:

Tidwell TJ. Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet. [Internet] [Masters thesis]. University of Utah; 2009. [cited 2020 Feb 19]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1658/rec/651.

Council of Science Editors:

Tidwell TJ. Insulin signaling in the hearts of uncoupling protein three knockout mice on a high fat diet. [Masters Thesis]. University of Utah; 2009. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/1658/rec/651

Texas A&M University

5. Rhoades, Ryan D. Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle.

Degree: 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2870

► Beef carcass value is influenced by the quantity and distribution of adipose tissue. Elucidation of metabolic controls of caloric partitioning between adipose depots could lead… (more)

▼ Beef carcass value is influenced by the quantity and distribution of adipose tissue. Elucidation of metabolic controls of caloric partitioning between adipose depots could lead to development of production solutions that enhance beef carcass value. Historical trends in Choice and Select beef supply and short-term demand structures for Choice and Select boxed beef were explored. Recent stabilization in slaughter mix may suggest an optimum is being approached. Evaluation of short-run demand supports this premise, and suggests that Choice and Select products may not be strong substitutes. Growth-based prediction equations relating carcass traits to growth traits using ultrasound measurements as the basis of projections under different growing systems were explored. Accuracy of carcass fat predictions from growth-based equations is influenced by weight gain between ultrasound and endpoint, breed, and gender; scans out to 120 d pre-harvest may be accurate. Angus steers were used to test effects of dietary energy source on muscle and adipose tissue metabolism and insulin sensitivity. Results suggest that feeding hay limited both glucose supply and tissue capacity to increase glucose utilization in response to insulin without altering acetate conversion to fatty acids. Because subcutaneous (s.c.) adipose tissue consistently utilized more acetate and oxidized more glucose than intramuscular (i.m.), these results suggest that hay-based diets may alter i.m. adipose tissue metabolism with less impact on s.c. adipose tissue. Additionally, s.c. adipose tissue may become resistant to insulin in steers fed to an excessive s.c. fat thickness. A final experiment was designed to test the effects of dietary energy source during backgrounding and compositional endpoint on adipose tissue metabolism and insulin sensitivity. Feeding hay during backgrounding may have differential effects on tissue lipogenesis. Feeding hay increased both glucose oxidation and incorporation of acetate into fatty acids; in i.m. insulin failed to stimulate glucose conversion to lipid. As physiological maturity increases, glucose conversion to CO2 and lactate increased, but the ability of insulin to stimulate lipid synthesis from glucose may be reduced. These data provide foundation for a hypothesis regarding diet-mediated regulation of differential adipose tissue metabolism. Validation of these hypotheses could generate nutritional strategies that alter the rate and site of adipose deposition. Advisors/Committee Members: Sawyer, Jason E. (advisor), Anderson, David P. (committee member), Lunt, David K. (committee member), Smith, Stephen B. (committee member).

Subjects/Keywords: Insulin; Cattle

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APA (6^th Edition):

Rhoades, R. D. (2009). Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2870

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rhoades, Ryan D. “Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle.” 2009. Thesis, Texas A&M University. Accessed February 19, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2870.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rhoades, Ryan D. “Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle.” 2009. Web. 19 Feb 2020.

Vancouver:

Rhoades RD. Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle. [Internet] [Thesis]. Texas A&M University; 2009. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2870.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rhoades RD. Influence of dietary energy source on in vitro substrate utilization and insulin sensitivity of muscle and adipose tissue of beef cattle. [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2870

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University

6. Papaioannou, Stamatios Evangelos. Studies of the functional tyrosyl residues of insulin.

Degree: PhD, Chemistry, 1966, Oregon State University

URL: http://hdl.handle.net/1957/47023

► Acetylimidazole was used to acetylate the tyrosyl residues of insulin. The kinetics of acetylation were studied by termination of the reaction at several time intervals,… (more)

▼ Acetylimidazole was used to acetylate the tyrosyl residues of insulin. The kinetics of acetylation were studied by termination of the reaction at several time intervals, isolation of acetylated insulin and determination of 0-acetyltyrosyl groups by deacetylation with hydroxylamine. The deacetylation was also studied kinetically by means of the absorbancy change during the reaction. The degree of availability of the tyrosyl groups in native insulin, and of the 0-acetyltyrosyl groups in the acetylated insulin was studied by the above kinetic studies. Two tyrosyl residues were acetylated at a rate sufficiently more fast than the remaining two so that a diacetyl derivative could be isolated. This preparation was fully active. The completely acetylated insulin was only thirty percent as active as native insulin in the mouse convulsion test. Native and acetylated insulin were inactivated by seventy percent on treatment with hydroxylamine. These and other findings lead to the conclusion that one or both of the slowly acetylated tyrosyl residues of insulin are involved in the mechanism of action of the hormone. In order to determine the location of the two acetylated tyrosyl residues, the diacetyl derivative of insulin was oxidized and the A and B chains isolated were assayed for acetyl groups. The diacetyl derivative was also digested separately with trypsin and chymotrypsin, and each core was also assayed for acetyl groups. From the results of these assays it was concluded that the diacetyl derivative of insulin was acetylated to the A19 and B16 tyrosyl residues, which are characterized as reactive, while the other two tyrosyl residues, A14 and B26 are non-reactive or bound. The fact that both tyrosyl B26, and asparaginyl A21 are bound and essential for hormone activity suggests a specific tyrosyl B26-carboxylate A21 interaction essential for maintaining the native conformation and the activity of insulin. The usefulness of the kinetic and structural studies employed here for evaluation of the degree of exposure of tyrosyl residues, selective blocking of tyrosyl groups, and determination of the location of reactive and non-reactive tyrosyl residues of insulin, for the purpose of structure-and-function studies on other problems, is discussed. Advisors/Committee Members: Becker, Robert R. (advisor).

Subjects/Keywords: Insulin

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APA (6^th Edition):

Papaioannou, S. E. (1966). Studies of the functional tyrosyl residues of insulin. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/47023

Chicago Manual of Style (16^th Edition):

Papaioannou, Stamatios Evangelos. “Studies of the functional tyrosyl residues of insulin.” 1966. Doctoral Dissertation, Oregon State University. Accessed February 19, 2020. http://hdl.handle.net/1957/47023.

MLA Handbook (7^th Edition):

Papaioannou, Stamatios Evangelos. “Studies of the functional tyrosyl residues of insulin.” 1966. Web. 19 Feb 2020.

Vancouver:

Papaioannou SE. Studies of the functional tyrosyl residues of insulin. [Internet] [Doctoral dissertation]. Oregon State University; 1966. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1957/47023.

Council of Science Editors:

Papaioannou SE. Studies of the functional tyrosyl residues of insulin. [Doctoral Dissertation]. Oregon State University; 1966. Available from: http://hdl.handle.net/1957/47023

McGill University

7. Lai, Wei H. Characterization of growth Factor Receptors in Human Placental Cells in Culture.

Degree: PhD, Department of of Experimental Medicine, 1984, McGill University

URL: http://digitool.library.mcgill.ca/thesisfile154093.pdf

►

The characteristics and specificity of receptors for insulin, epidermal growth factor (EGF), and the insulin-like growth factors (IGFs), IGF-I and IGF-II, were studied in human… (more)

Subjects/Keywords: Insulin

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APA (6^th Edition):

Lai, W. H. (1984). Characterization of growth Factor Receptors in Human Placental Cells in Culture. (Doctoral Dissertation). McGill University. Retrieved from http://digitool.library.mcgill.ca/thesisfile154093.pdf

Chicago Manual of Style (16^th Edition):

Lai, Wei H. “Characterization of growth Factor Receptors in Human Placental Cells in Culture.” 1984. Doctoral Dissertation, McGill University. Accessed February 19, 2020. http://digitool.library.mcgill.ca/thesisfile154093.pdf.

MLA Handbook (7^th Edition):

Lai, Wei H. “Characterization of growth Factor Receptors in Human Placental Cells in Culture.” 1984. Web. 19 Feb 2020.

Vancouver:

Lai WH. Characterization of growth Factor Receptors in Human Placental Cells in Culture. [Internet] [Doctoral dissertation]. McGill University; 1984. [cited 2020 Feb 19]. Available from: http://digitool.library.mcgill.ca/thesisfile154093.pdf.

Council of Science Editors:

Lai WH. Characterization of growth Factor Receptors in Human Placental Cells in Culture. [Doctoral Dissertation]. McGill University; 1984. Available from: http://digitool.library.mcgill.ca/thesisfile154093.pdf

Oregon State University

8. Wu, Lily Henson Liu. Preparation and properties of polyglycyl insulin.

Degree: MS, Chemistry, 1966, Oregon State University

URL: http://hdl.handle.net/1957/47267

► In order to understand more about insulin behavior in solution, Zn-free insulin was modified by adding polyglycyl chains to the molecule and then observing the… (more)

Subjects/Keywords: Insulin

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APA (6^th Edition):

Wu, L. H. L. (1966). Preparation and properties of polyglycyl insulin. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/47267

Chicago Manual of Style (16^th Edition):

Wu, Lily Henson Liu. “Preparation and properties of polyglycyl insulin.” 1966. Masters Thesis, Oregon State University. Accessed February 19, 2020. http://hdl.handle.net/1957/47267.

MLA Handbook (7^th Edition):

Wu, Lily Henson Liu. “Preparation and properties of polyglycyl insulin.” 1966. Web. 19 Feb 2020.

Vancouver:

Wu LHL. Preparation and properties of polyglycyl insulin. [Internet] [Masters thesis]. Oregon State University; 1966. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1957/47267.

Council of Science Editors:

Wu LHL. Preparation and properties of polyglycyl insulin. [Masters Thesis]. Oregon State University; 1966. Available from: http://hdl.handle.net/1957/47267

University of Debrecen

9. Németh, Anna. A cukorbetegség és a lipid anyagcsere zavarainak összefüggései .

Degree: DE – TEK – Természettudományi és Technológiai Kar – Biológiai és Ökológiai Intézet, 2011, University of Debrecen

URL: http://hdl.handle.net/2437/108264

► A dolgozatban arra kerestem a választ, hogy mi történik a lipid anyagcserével diabetes mellitus során és azokat a tényezőket is, amelyeknek igazolódik a betegség létrejöttében… (more)

Subjects/Keywords: diabetes; insulin

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APA (6^th Edition):

Németh, A. (2011). A cukorbetegség és a lipid anyagcsere zavarainak összefüggései . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/108264

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Németh, Anna. “A cukorbetegség és a lipid anyagcsere zavarainak összefüggései .” 2011. Thesis, University of Debrecen. Accessed February 19, 2020. http://hdl.handle.net/2437/108264.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Németh, Anna. “A cukorbetegség és a lipid anyagcsere zavarainak összefüggései .” 2011. Web. 19 Feb 2020.

Vancouver:

Németh A. A cukorbetegség és a lipid anyagcsere zavarainak összefüggései . [Internet] [Thesis]. University of Debrecen; 2011. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/2437/108264.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Németh A. A cukorbetegség és a lipid anyagcsere zavarainak összefüggései . [Thesis]. University of Debrecen; 2011. Available from: http://hdl.handle.net/2437/108264

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

10. Golkaran, Donya. In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin .

Degree: Chemical Engineering, 2013, Queens University

URL: http://hdl.handle.net/1974/8211

► The aim of this study was to evaluate the factors, which affect insulin release and stability in simulated gastrointestinal fluid that ultimately will reduce the… (more)

▼ The aim of this study was to evaluate the factors, which affect insulin release and stability in simulated gastrointestinal fluid that ultimately will reduce the bioavailability of insulin in a nanoparticulate oral delivery system. The focus was on nanoparticulate carriers developed by C. Reis, which have the highest level of bioavailability reported in the literature thus far. Particles observed by TEM were spherical and particle analyzer data showed that the peak of the distribution was 10 nm. Entrapment efficiency of insulin was 85%. Insulin retention/release was evaluated in both enzymatic and enzyme-free simulated digestive ﬂuids. HPLC measurement showed that insulin was stable in acid condition in presence and absence of pepsin. By changing the pH to 6.8 in an intestinal simulation, the amount of insulin decreased such that at the end of the 5 h simulation, 71% of the insulin was measureable in simulated GI fluid in presence of enzymes. Insulin release profile from nanoparticles was low in gastric condition. After changing the pH to 6.8, an initial release of insulin occurred in the first 1h followed by plateau state in the remaining 2h. After a total of 5h in acidic followed by neutral pH medium, the formulation retained 48% of the insulin in the particles in simulated GI fluid in presence of enzyme. As confirmation of the amount of retained insulin, after 5h, particles were dissolved and the formulation was shown to fully retain up to 45% of the insulin in extended simulated gastrointestinal condition in the presence of enzymes. Insulin release behavior was investigated in different simulated small intestinal media by incorporating phosphate buffer or bicarbonate buffer and physiological electrolytes. The release rate from particles in the phosphate buffer was faster compared to bicarbonate buffers. KBB-C showed a release profile that was very different from other media, with about 10% released in the first 30 min and 70% of the insulin remaining entrapped within the particles at the end of the experiment. Release in this buffer was reduced due to the decreased sodium to calcium ratio compared to the other KBB media.

Subjects/Keywords: Insulin Delivery

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Golkaran, D. (2013). In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/8211

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Golkaran, Donya. “In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin .” 2013. Thesis, Queens University. Accessed February 19, 2020. http://hdl.handle.net/1974/8211.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Golkaran, Donya. “In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin .” 2013. Web. 19 Feb 2020.

Vancouver:

Golkaran D. In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin . [Internet] [Thesis]. Queens University; 2013. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/1974/8211.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Golkaran D. In Vitro Simulation of In Vivo Performance of Oral Dosed Nanoparticulate Insulin . [Thesis]. Queens University; 2013. Available from: http://hdl.handle.net/1974/8211

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Louisiana State University

11. Lestelle, Jeanne D. Insulin dose response curves and factors affecting insulin sensitivity in horses.

Degree: MS, Animal Sciences, 2012, Louisiana State University

URL: etd-04162012-115502 ; https://digitalcommons.lsu.edu/gradschool_theses/1016

► Three experiments were conducted to further study the use of intravenous insulin injection to measure insulin sensitivity in horses. In the first experiment, glucose… (more)

▼ Three experiments were conducted to further study the use of intravenous insulin injection to measure insulin sensitivity in horses. In the first experiment, glucose responses to multiple doses of recombinant human insulin were compared in insulin sensitive and insensitive mares. Regression lines describing the responses in insensitive mares had less (P = 0.003) steep slopes and greater (P = 0.006) effective doses at 50% response (ED50) compared to sensitive mares. Curvilinear regression models provided a good fit (R2 = 0.95) for the prediction of ED50 from the individual responses to 50 mU/kg BW insulin. The second experiment estimated the repeatability of the glucose responses to a fixed dose of insulin in 41 horses (mares and geldings) injected twice, between 7 and 14 days apart. Overall agreement between the responses was significant (P < 0.001) but not high enough to be predictive (R2 value = 0.384). Intra-horse coefficients of variation (CV) ranged from 0 to 68.7%, and averaged 23%. Mares and geldings were similar in their repeatabilities. Horses in the bottom half of the sensitivity rankings had a greater (P = 0.03) average intra-horse CV (28.7 ± 4.6%) than horses in the top half (16.7 ± 2.2%). In the third experiment (single switch-back design), glucose responses to a fixed dose of insulin were compared after an overnight (about 12 hours) versus a 24-hour period of feed deprivation in geldings previously determined to be insulin sensitive (n = 4) versus insensitive (n = 4). The longer period of feed deprivation decreased (P = 0.06) the percentage decrease in blood glucose concentrations, indicating a lesser sensitivity relative to the 12-hour period of deprivation. Insulin sensitivity also affected (P = 0.0003) the glucose response, with sensitive geldings exhibiting the greater response. It was concluded that the response to a single dose of insulin is often a good predictor of a horse's insulin sensitivity, but that the lack of repeatability in some horses could lead to errors in diagnosis. The decrease in glucose response seen after 24 hours of feed deprivation is likely due to the elevation of fatty acid concentrations in the blood.

Subjects/Keywords: insulin; horse; insulin sensitivity; glucose tolerance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lestelle, J. D. (2012). Insulin dose response curves and factors affecting insulin sensitivity in horses. (Masters Thesis). Louisiana State University. Retrieved from etd-04162012-115502 ; https://digitalcommons.lsu.edu/gradschool_theses/1016

Chicago Manual of Style (16^th Edition):

Lestelle, Jeanne D. “Insulin dose response curves and factors affecting insulin sensitivity in horses.” 2012. Masters Thesis, Louisiana State University. Accessed February 19, 2020. etd-04162012-115502 ; https://digitalcommons.lsu.edu/gradschool_theses/1016.

MLA Handbook (7^th Edition):

Lestelle, Jeanne D. “Insulin dose response curves and factors affecting insulin sensitivity in horses.” 2012. Web. 19 Feb 2020.

Vancouver:

Lestelle JD. Insulin dose response curves and factors affecting insulin sensitivity in horses. [Internet] [Masters thesis]. Louisiana State University; 2012. [cited 2020 Feb 19]. Available from: etd-04162012-115502 ; https://digitalcommons.lsu.edu/gradschool_theses/1016.

Council of Science Editors:

Lestelle JD. Insulin dose response curves and factors affecting insulin sensitivity in horses. [Masters Thesis]. Louisiana State University; 2012. Available from: etd-04162012-115502 ; https://digitalcommons.lsu.edu/gradschool_theses/1016

Deakin University

12. Holmes-Truscott, Elizabeth. Receptiveness and resistance: perceptions of insulin use in type 2 diabetes.

Degree: School of Psychology, 2016, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30097451

► The aim of this thesis was to investigate attitudes to insulin therapy among Australian adults with type 2 diabetes. Using a mixed methods approach, this… (more)

Subjects/Keywords: psychological insulin resistance (PIR); diabetes; insulin therapy

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APA (6^th Edition):

Holmes-Truscott, E. (2016). Receptiveness and resistance: perceptions of insulin use in type 2 diabetes. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30097451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Holmes-Truscott, Elizabeth. “Receptiveness and resistance: perceptions of insulin use in type 2 diabetes.” 2016. Thesis, Deakin University. Accessed February 19, 2020. http://hdl.handle.net/10536/DRO/DU:30097451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Holmes-Truscott, Elizabeth. “Receptiveness and resistance: perceptions of insulin use in type 2 diabetes.” 2016. Web. 19 Feb 2020.

Vancouver:

Holmes-Truscott E. Receptiveness and resistance: perceptions of insulin use in type 2 diabetes. [Internet] [Thesis]. Deakin University; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10536/DRO/DU:30097451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Holmes-Truscott E. Receptiveness and resistance: perceptions of insulin use in type 2 diabetes. [Thesis]. Deakin University; 2016. Available from: http://hdl.handle.net/10536/DRO/DU:30097451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Univerzitet u Beogradu

13. Cvijović, Goran M., 1971-. Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma.

Degree: Medicinski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:12592/bdef:Content/get

►

INTERNA MEDICINA - ENDOKRINOLOGIJA / INTERNAL MEDICINE - ENDOCRINOLOGY

Uvod i cilj: Prethodno je uočeno postojanje insulinske rezistencije i povećana prevalenca oštećene tolerancije na glikozu… (more)

▼

INTERNA MEDICINA - ENDOKRINOLOGIJA / INTERNAL MEDICINE - ENDOCRINOLOGY

Uvod i cilj: Prethodno je uočeno postojanje insulinske rezistencije i povećana prevalenca oštećene tolerancije na glikozu i tipa 2 dijabetesa kod pacijenata sa primarnim hiperparatireoidizmom. Efekat paratireoidektomije na insulinsku senzitivnost je praćen kontraverznim nalazima u zavisnosti od metode koja je korištena za procenu insulinske senzitivnosti: nije bilo promene kada su korišteni HOMA i QUICKI dok je Minimalnim modelom pokazano značajno poboljšanje insulinske senzitivnosti.Cilj ovog rada je bio da se proceni insulinska senzitivnost pre i nakon paratireoidektomije kod pacijenata sa PHPT putem euglikemijskog hiperinsulinemijskog klampa. Materijal i metode: Kod 44 pacijenta sa PHPT i 11 zdravih kontrola komparabilne starosti i indeksa telesne mase procenjivali smo insulinsku senzitivnost (pomoću tehnike klampa, HOMA IR i ISI indeksa), insulinsku sekreciju (putem površine pod krivom za glikemije i insulinemije tokom OGTTa i izračunavajući akutni insulinski odgovor iz podataka dobijenih IVGTTom), lipidni profil i nivo hsCRP kao marker hronične inflamacije. Rezultati: Pre operacije vrednosti M indeksa i HOMA IR su ukazivale na postojanje insulinske rezistencije kod pacijenata sa PHPT. Nije bilo razlike u M indeksu (3.74±1.89 vs 4.62±2.27, p >0.05), HOMA IR (2.94±1.39 vs. 3.29±0.81, p > 0.05), AUC glikoze (863.0±261.3 vs 842.3±165.5, p>0.05), AUC insulina (7068.7±4159.0 vs 7229.6±2581.7, p>0.05), ISI (4.73±2.77 vs 4.25±2.94, p>0.05) i AIR (47.89±32.05 vs. 38.96±21.20, p>0.05) izmeĎu pacijenata sa PHPT i zdravih kontrola. Došlo je do značajnog poboljšanja insulinske senzitivnosti nakon operacije al ii preoperativna i postoperativna vrednost M indeksa se nisu razlikovale od zdravih kontrola. Nije uočena promena u HOMA IR, AUC za glikozu i insulin ISI i AIR, lipidima i hsCRP nakon operacije. Zaključak: Dobili smo značajno poboljšanje insulinske senzitivnosti nakon paratireoidektomije kod pacijenata sa PHPT koristeći klamp tehniku. Postoperativno nije do došlo do značajne promene u drugim pokazateljima insulinske senzitivnosti, paramtrima insulinske sekrecije, lipidima i hsCRP.

Advisors/Committee Members: Micić, Dragan, 1950-.

Subjects/Keywords: primary hyperparathyroidism; insulin sensitivity; insulin secretion

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APA (6^th Edition):

Cvijović, Goran M., 1. (2016). Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:12592/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cvijović, Goran M., 1971-. “Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma.” 2016. Thesis, Univerzitet u Beogradu. Accessed February 19, 2020. https://fedorabg.bg.ac.rs/fedora/get/o:12592/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cvijović, Goran M., 1971-. “Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma.” 2016. Web. 19 Feb 2020.

Vancouver:

Cvijović, Goran M. 1. Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2020 Feb 19]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12592/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cvijović, Goran M. 1. Sekrecija insulina i insulinska senzitivnost perifernih tkiva pre i nakon radikalnog lečenja primarnog hiperparatireoidizma. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:12592/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Mississippi State University

14. Ramdas, Maya. CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE.

Degree: PhD, Biological Sciences, 2009, Mississippi State University

URL: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07232009-102440/ ;

► Molecular analysis of the cross talk between Angiotensin II (Ang II) and insulin signaling systems reveal that they are multifaceted and occur at cellular… (more)

▼ Molecular analysis of the cross talk between Angiotensin II (Ang II) and insulin signaling systems reveal that they are multifaceted and occur at cellular level and intracellular level. Experiments were carried out to evaluate the crosstalk between the Ang II receptors-AT1 and AT2 and the Insulin Receptor (IR) to understand the changes in the signaling pathway that could lead to the transition from hypertension to insulin resistance. Transient expression of rat AT2 in CHO cells induced co-immunoprecipitation of the AT2R with IRâ and inhibition of IRâ tyrosine phosphorylation. An AT2-peptide carrying the amino acids 226-363 (that spans 3^rd intracellular loop (ICL) and C-terminal cytoplasmic domain) was sufficient for AT2- IRâ interaction in a yeast two-hybrid assay. An orthovanadate-insensitive AT2- IRâ association was also observed in human breast cancer cell line MCF-7. Interestingly, while AT2- IRâ complex formation was insensitive to pertussis toxin (PTX), AT2-mediated inhibition of IRâ phosphorylation was partially sensitive to PTX treatment in MCF-7. To address the mechanism behind the transition of an early hypertensive heart to an insulin resistant status, we investigated the changes that occur at post translational level in the IR and its downstream signaling molecules that modulate insulin signaling. Early hypertension was induced in 10-week old SD rats by 2% NaCl diet in combination with Ang II infusion. Enhanced serine phosphorylation of the IRâ suggestive of dysfunctional insulin signaling was observed in cardiac tissues as a result of the treatment. In addition, an enhanced association of both AT1R and AT2R with IRâ was observed in the heart tissue lysates from hypertensive rat heart. To evaluate the tissue effects of Ang II, we compared the transcriptome of hypertensive rat hearts to the controls. Analysis suggests that the Ang II induces multiple responses in heart tissue that result in changes to the gene expression pattern intended to promote insulin sensitivity and insulin resistance. Taken together our results suggest that exogenous Ang II and moderately high salt diet promote metabolic abnormalities in heart tissue that result in sequestration of IR and modulation of IR signaling, and significant changes in gene expression profile in the hypertensive heart. Advisors/Committee Members: Dwayne Wise (committee member), Donna Gordon (committee member), Nara Gavini (committee member), John Boyle (committee member), Lakshmi Pulakat (chair).

Subjects/Keywords: Angiotensin II; Insulin; Hypertension; Insulin Resistance; Signaling

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APA (6^th Edition):

Ramdas, M. (2009). CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE. (Doctoral Dissertation). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-07232009-102440/ ;

Chicago Manual of Style (16^th Edition):

Ramdas, Maya. “CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE.” 2009. Doctoral Dissertation, Mississippi State University. Accessed February 19, 2020. http://sun.library.msstate.edu/ETD-db/theses/available/etd-07232009-102440/ ;.

MLA Handbook (7^th Edition):

Ramdas, Maya. “CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE.” 2009. Web. 19 Feb 2020.

Vancouver:

Ramdas M. CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE. [Internet] [Doctoral dissertation]. Mississippi State University; 2009. [cited 2020 Feb 19]. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07232009-102440/ ;.

Council of Science Editors:

Ramdas M. CROSSTALK BETWEEN ANGIOTENSIN II RECEPTORS AND INSULIN RECEPTOR: A POSSIBLE MECHANISM FOR THE CO-DEVELOPMENT OF HYPERTENSION AND INSULIN RESISTANCE. [Doctoral Dissertation]. Mississippi State University; 2009. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-07232009-102440/ ;

University of British Columbia

15. Verchere, Cameron Bruce. Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 .

Degree: 1987, University of British Columbia

URL: http://hdl.handle.net/2429/26657

► The effect of varying concentrations of glucose or the gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and somatostatin (SS-14), on the in vitro immunoreactive insulin (IRI)… (more)

▼ The effect of varying concentrations of glucose or the gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and somatostatin (SS-14), on the in vitro immunoreactive insulin (IRI) response to the parasympathetic neurotransmitter, acetylcholine (ACh) was investigated. The isolated, vascularly perfused rat pancreas was used in all experiments. Acetylcholine (1.0 µM) did not stimulate IRI secretion in the presence of 2.2 mM glucose. However, in the presence of 4.4, 6.6, or 8.9 mM glucose, ACh (1.0 µM) potently stimulated IRI secretion (approximately fourfold). At a higher glucose concentration (17.8 mM), the IRI response to ACh was reduced. GIP also potentiated the IRI response to 1.0 µM ACh. This potentiation was most marked in the presence of 1.0 nM GIP, whereas the effect of concomitant infusion of 0.2 nM GIP and 1.0 µM ACh was only slightly greater than additive. SS-14 potently inhibited ACh-stimulated IRI secretion. These results demonstrated the glucose dependency of cholinergically stimulated IRI secretion, and that physiological levels of glucose and GIP increased B-cell sensitivity to cholinergic stimulation. It was suggested that the parasympathetic stimulation of IRI secretion associated with food intake could be affected by postprandial increases in glucose, GIP, and SS-14. The idea that endogenously released somatostatin may have influenced glucose or GIP-stimulated IRI secretion was not supported by the present experiments, since neither glucose (8.9 mM) nor GIP (2.0 nM) were found to have a significant effect on the release of pancreatic somatostatin-like immunoreactivity (SLI). Both atropine (1.0 µM) and hexamethonlum (100 µM) inhibited the IRI response to ACh. This suggested that the parasympathetic stimulation of IRI secretion was mediated not only by muscarinic receptors on the B-cell, but also by nicotinic receptors on intrapancreatic ganglia. Neither atropine nor hexamethonlum had a significant effect on glucose- or GIP-stimulated IRI secretion, indicating that the IRI response to these stimuli was not mediated by cholinergic receptors. Both SS-14 and the synthetic somatostatin analog SMS 201-995 (SMS; Sandostatin®) inhibited IRI secretion stimulated by 8.9 mM glucose, 2.0 nM GIP, or 1;.0 µM ACh, but not 17.8 mM glucose. The most potent inhibition by both SS-14 and SMS was observed in the presence of the weakest IRI stimuli (8.9 mM glucose and 1.0 µM ACh). These results suggested that the inhibitory effects of somatostatin on the B-cell could be overcome by the presence of strong stimuli. In addition, the inhibitory effects of the native hormone and the analog were found to be approximately equipotent (weight basis), indicating that the increased potency of SMS previously observed in vivo was due to its longer half-life in plasma, and not due to a more potent direct effect on the B-cell.

Subjects/Keywords: Insulin; Insulin resistance

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APA (6^th Edition):

Verchere, C. B. (1987). Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 . (Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/26657

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Verchere, Cameron Bruce. “Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 .” 1987. Thesis, University of British Columbia. Accessed February 19, 2020. http://hdl.handle.net/2429/26657.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Verchere, Cameron Bruce. “Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 .” 1987. Web. 19 Feb 2020.

Vancouver:

Verchere CB. Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 . [Internet] [Thesis]. University of British Columbia; 1987. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/2429/26657.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Verchere CB. Control of insulin secretion from the perfused rat pancreas : effects of acetylcholine and a somatostatin analog, SMS 201-995 . [Thesis]. University of British Columbia; 1987. Available from: http://hdl.handle.net/2429/26657

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht

16. Dopper, I. Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients.

Degree: 2014, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/292970

► The relationship between diabetes and the risk for cancer development seems to be more and more confirmed. An important link between these two is the… (more)

Subjects/Keywords: Insulin; Cancer; Diabetes

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APA (6^th Edition):

Dopper, I. (2014). Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/292970

Chicago Manual of Style (16^th Edition):

Dopper, I. “Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients.” 2014. Masters Thesis, Universiteit Utrecht. Accessed February 19, 2020. http://dspace.library.uu.nl:8080/handle/1874/292970.

MLA Handbook (7^th Edition):

Dopper, I. “Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients.” 2014. Web. 19 Feb 2020.

Vancouver:

Dopper I. Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients. [Internet] [Masters thesis]. Universiteit Utrecht; 2014. [cited 2020 Feb 19]. Available from: http://dspace.library.uu.nl:8080/handle/1874/292970.

Council of Science Editors:

Dopper I. Diabetes, insulin and cancer risk The molecular role of insulin signaling and hyperinsulinemia in cancer development and progression in diabetes patients. [Masters Thesis]. Universiteit Utrecht; 2014. Available from: http://dspace.library.uu.nl:8080/handle/1874/292970

University of Hong Kong

17. Liu, Wenjing. Modulatory effect of gut microbiota on insulin sensitivity.

Degree: Master of Medical Sciences, 2017, University of Hong Kong

URL: http://hdl.handle.net/10722/251331

►

Gut microbiota is indispensable in regulating host metabolism. Current research focus on the role of gut microbiota in the progression of obesity, which is associated… (more)

▼

Gut microbiota is indispensable in regulating host metabolism. Current research focus on the role of gut microbiota in the progression of obesity, which is associated with numerous complications, including diabetes mellitus and cardiovascular diseases. The global prevalence of diabetes mellitus dramatically escalate in modern society. Altered gut microbiota has been identified in type 2 diabetic patients, suggesting gut microbiota may be involved in the development of type 2 diabetes mellitus. Furthermore, animal studies have demonstrated that gut microbial species could alleviate body weight and insulin resistance in obese mice. However, whether the improvement of insulin sensitivity is due to the direct modulatory effects of gut microbiota or it is the secondary effects of body weight loss still remains unknown. Adiponectin, one of the most abundant adipokines secreted from adipocytes, possesses versatile functions against a cluster of metabolic disorders including insulin resistance, fatty liver and cardiovascular diseases. What’s more, adiponectin knock out (ADN KO) mice develop severe insulin resistance compared to their wild type (WT) littermates after high fat diet (HFD) treatment. Interestingly, body weight is comparable between WT mice and ADN KO mice after HFD treatment. In this study, we used ADN KO mice to investigate the modulatory effects of gut microbiota on insulin sensitivity. Both ADN KO mice and their WT littermates were fed on either normal chow diet (NCD) and HFD for 12 weeks. Consistent with previous finding, long-term HFD treatment led to a severe insulin resistance in ADN KO mice compared to their WT littermates. In order to further explore the modulatory effect of gut microbiota on insulin sensitivity, fecal microbiota transplantation was performed. Recipient receiving microbes from ADN KO mice fed on HFD develop severe insulin resistance compared to recipient receiving microbes from WT littermates fed on HFD. Collectively, our results reveal that gut microbiota from ADN KO mice fed on HFD is sufficient to modulate insulin sensitivity in recipients, suggesting the direct regulatory effects of gut microbiota on insulin sensitivity.

published_or_final_version

Medicine

Master

Master of Medical Sciences

Subjects/Keywords: Insulin; Intestines - Microbiology

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APA (6^th Edition):

Liu, W. (2017). Modulatory effect of gut microbiota on insulin sensitivity. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/251331

Chicago Manual of Style (16^th Edition):

Liu, Wenjing. “Modulatory effect of gut microbiota on insulin sensitivity.” 2017. Masters Thesis, University of Hong Kong. Accessed February 19, 2020. http://hdl.handle.net/10722/251331.

MLA Handbook (7^th Edition):

Liu, Wenjing. “Modulatory effect of gut microbiota on insulin sensitivity.” 2017. Web. 19 Feb 2020.

Vancouver:

Liu W. Modulatory effect of gut microbiota on insulin sensitivity. [Internet] [Masters thesis]. University of Hong Kong; 2017. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10722/251331.

Council of Science Editors:

Liu W. Modulatory effect of gut microbiota on insulin sensitivity. [Masters Thesis]. University of Hong Kong; 2017. Available from: http://hdl.handle.net/10722/251331

Deakin University

18. Holmes-Truscott, Elizabeth. Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes.

Degree: 2016, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30096807

► The aim of this thesis was to investigate attitudes to insulin therapy among Australian adults with type 2 diabetes. Using a mixed methods approach, this… (more)

Subjects/Keywords: diabetes; insulin therapy

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APA (6^th Edition):

Holmes-Truscott, E. (2016). Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30096807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Holmes-Truscott, Elizabeth. “Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes.” 2016. Thesis, Deakin University. Accessed February 19, 2020. http://hdl.handle.net/10536/DRO/DU:30096807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Holmes-Truscott, Elizabeth. “Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes.” 2016. Web. 19 Feb 2020.

Vancouver:

Holmes-Truscott E. Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes. [Internet] [Thesis]. Deakin University; 2016. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10536/DRO/DU:30096807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Holmes-Truscott E. Receptiveness and resistance: perceptions of insulin use in Type 2 diabetes. [Thesis]. Deakin University; 2016. Available from: http://hdl.handle.net/10536/DRO/DU:30096807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Debrecen

19. Chandan, Amar Paul Singh. Diabetes Mellitus and the implications of modern insulin therapies .

Degree: DE – Általános Orvostudományi Kar, 2014, University of Debrecen

URL: http://hdl.handle.net/2437/194936

► This thesis was written with the purpose of investigating the current litterature available on the subject of insulin analogues. Recently a plethora of molecularly modified… (more)

Subjects/Keywords: Diabetes Mellitus; Insulin

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APA (6^th Edition):

Chandan, A. P. S. (2014). Diabetes Mellitus and the implications of modern insulin therapies . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/194936

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chandan, Amar Paul Singh. “Diabetes Mellitus and the implications of modern insulin therapies .” 2014. Thesis, University of Debrecen. Accessed February 19, 2020. http://hdl.handle.net/2437/194936.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chandan, Amar Paul Singh. “Diabetes Mellitus and the implications of modern insulin therapies .” 2014. Web. 19 Feb 2020.

Vancouver:

Chandan APS. Diabetes Mellitus and the implications of modern insulin therapies . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/2437/194936.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chandan APS. Diabetes Mellitus and the implications of modern insulin therapies . [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/194936

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Smith, Zachary K. F. The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves.

Degree: MS, Animal Science, 2015, South Dakota State University

URL: https://openprairie.sdstate.edu/etd/1978

► A series of experiments were conducted to evaluate the influence of supplemental dietary chromium (0 or 400 ppb) on insulin responsiveness in finishing steers… (more)

▼ A series of experiments were conducted to evaluate the influence of supplemental dietary chromium (0 or 400 ppb) on insulin responsiveness in finishing steers (Exp 1. and Exp 2.), and energy status in newly weaned steers upon introduction to the feedlot (Exp 3.). To evaluate insulin responsiveness, two models were used with finished steers of different ages: Exp 1. 12 steers; 24 mo old (BW=783 ± 29 kg); and Exp 2. 24 steers; 14 mo old (BW=625 ± 24 kg). A jugular infusion of insulin (0.45 IU bovine insulin/ kg of BW0.75, INS) was pulse dosed 2 h post-prandial. A jugular infusion of PBS (SHAM) was included in Exp. 2. Blood samples were collected at -30, 120, 195, 255, and 315 min) relative to the morning feed delivery after 84 d (Exp 1.) and 86 d (Exp 2.) on test diets. No diet x time interactions were detected for any plasma metabolites in old or young steers. In Exp 2., INS effectively cleared plasma glucose (GLS). Diet had no impact on changes in GLS in Exp 2. Diet had no impact (P > 0.20) on plasma concentrations of insulin in either experiment. In Exp 2., there tended (P=0.10) to be a diet x insulin interaction for post-infusion insulin levels. Insulin values were similar for all steers at (t195) and (t315) and elevated at (t255) for non-Cr fed steers subjected to INS. At t120, CrP caused greater (P < 0.05) plasma urea-N (PUN) concentrations when compared to CON in Exp 1. but not in Exp 2. Effects of Cr on PUN in Exp 1. may be due to improved insulin sensitivity affecting AA uptake in the peripheral tissue of old, heavy steers. In Exp 3., there were no diet x day interactions (P>0.20) for GLS, insulin, or PUN. The GLS and PUN levels were similar between diets (P > 0.20). Insulin levels were higher (P0.20) between diets on d 5 and higher (P < 0.05) on d 12 in calves fed CrP. The shift in NEFA on d 12 coincided with a spike in insulin levels. Both events occurred at the time that NEG intake was approaching the acclimated plateau and neither event impacted glucose status. The effective use of chromium in feedlot diets is likely dictated by age dependent differences in insulin sensitivity, metabolite needs for growth, and the degree of stress that ultimately result in a chromium deficient state. Advisors/Committee Members: Robbi H. Pritchard.

Subjects/Keywords: chromium; insulin; steers

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APA (6^th Edition):

Smith, Z. K. F. (2015). The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves. (Masters Thesis). South Dakota State University. Retrieved from https://openprairie.sdstate.edu/etd/1978

Chicago Manual of Style (16^th Edition):

Smith, Zachary K F. “The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves.” 2015. Masters Thesis, South Dakota State University. Accessed February 19, 2020. https://openprairie.sdstate.edu/etd/1978.

MLA Handbook (7^th Edition):

Smith, Zachary K F. “The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves.” 2015. Web. 19 Feb 2020.

Vancouver:

Smith ZKF. The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves. [Internet] [Masters thesis]. South Dakota State University; 2015. [cited 2020 Feb 19]. Available from: https://openprairie.sdstate.edu/etd/1978.

Council of Science Editors:

Smith ZKF. The Evaluation of Chromium Propionate Supplementation on Insulin Responsiveness in Finishing Steers and Energy Status in Newly Weaned Steer Calves. [Masters Thesis]. South Dakota State University; 2015. Available from: https://openprairie.sdstate.edu/etd/1978

Vanderbilt University

21. Speed, Nicole Kathryn. The Role of Insulin Signaling on Dopamine Transporter Trafficking.

Degree: PhD, Pharmacology, 2010, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-07212010-144350/ ;

► Dopaminergic neurotransmission is a critical component in the regulation of several behaviors, including cognition, motor function, motivation, and reward. Abnormalities in dopamine (DA) signaling have… (more)

▼ Dopaminergic neurotransmission is a critical component in the regulation of several behaviors, including cognition, motor function, motivation, and reward. Abnormalities in dopamine (DA) signaling have been linked to several disorders, including schizophrenia, Parkinsonâs Disease, drug addiction, and eating disorders. An important component in regulating DA neurotransmission is the DA transporter (DAT), which controls the inactivation of DA signaling by uptake of DA from the synapse into the presynaptic bouton. This action depends upon the number of functional transporters expressed at the plasma membrane. As such, regulation of DAT cell surface expression is an important mechanism to modify DA neurotransmission. A growing body of literature indicates that insulin signaling, including the downstream effector protein kinase B (Akt), is an important regulator of DAT function by virtue of fine tuning the transporterâs cell surface expression. In this dissertation, I first sought to further define the insulin signaling pathway regulating DAT by identifying the isoform of Akt responsible for modulating DAT cell surface expression. The data shown here support that Akt2, the isoform believed to mediate insulin signaling, regulates DAT cell surface expression. Furthermore, we sought to understand whether high fat feeding, diet induced obesity (DIO) would cause a reduction in Akt phosphorylation in brain, and as a consequence, alter DAT function. Here I report that a high fat diet alters insulin signaling, namely Akt activity, and results in a reduction of DAT cell surface expression in the striatum. In addition, I demonstrate a functional reduction in DA clearance in vivo and a reduction in AMPH-induced locomotor activity. Upon viral rescue of insulin signaling via expression of insulin receptor substrate 2 (IRS2), DAT cell surface expression and AMPH-induced locomotor activity are restored. Collectively, these data demonstrate that insulin, by signaling through Akt2, regulates DAT function, and that a high fat diet leads to improper insulin signaling, thus altering DAT cell surface expression. Therefore, dysregulation of DA tone by alterations of DAT function is an important concern for individuals who have developed insulin resistance, and may have mechanistic implications for the co-morbid nature of obesity and neuropsychiatric disorders. Advisors/Committee Members: Aurelio Galli (committee member), Randy Blakely (chair), Gregg Stanwood (committee member), Kevin Niswender (committee member), Brian Wadzinski (committee member).

Subjects/Keywords: dopamine; insulin; obesity

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APA (6^th Edition):

Speed, N. K. (2010). The Role of Insulin Signaling on Dopamine Transporter Trafficking. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07212010-144350/ ;

Chicago Manual of Style (16^th Edition):

Speed, Nicole Kathryn. “The Role of Insulin Signaling on Dopamine Transporter Trafficking.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed February 19, 2020. http://etd.library.vanderbilt.edu/available/etd-07212010-144350/ ;.

MLA Handbook (7^th Edition):

Speed, Nicole Kathryn. “The Role of Insulin Signaling on Dopamine Transporter Trafficking.” 2010. Web. 19 Feb 2020.

Vancouver:

Speed NK. The Role of Insulin Signaling on Dopamine Transporter Trafficking. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2020 Feb 19]. Available from: http://etd.library.vanderbilt.edu/available/etd-07212010-144350/ ;.

Council of Science Editors:

Speed NK. The Role of Insulin Signaling on Dopamine Transporter Trafficking. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://etd.library.vanderbilt.edu/available/etd-07212010-144350/ ;

University of Missouri – Kansas City

22. Jain, Piyush K., 1985-. Light-activated biomacromolecules .

Degree: 2013, University of Missouri – Kansas City

URL: http://hdl.handle.net/10355/45499

► Biomacromolecules, mainly nucleic acids and proteins, are involved in every cellular process and therefore their aberrant level or function is linked with most of the… (more)

▼ Biomacromolecules, mainly nucleic acids and proteins, are involved in every cellular process and therefore their aberrant level or function is linked with most of the diseases. Controlling these macromolecules using light can therefore be immediately applied towards a range of biomedical fields including bioengineering, biotechnology, biochemistry, medicinal chemistry, diagnostics, therapeutics, and so on. In this dissertation, multiple approaches to create the photoactivable macromolecules and their applications in biomedical field are discussed. In the first part of this dissertation, optimization of light activated RNA interference (LARI), a technique developed earlier in our lab, is discussed. By modifying nucleic acid with various new photolabile groups, RNA interference (RNAi) was brought under the control of light. Using these novel caged macromolecules, gene expression was patterned in cell monolayers, demonstrating the potential of LARI in controlling the spacing, timing and extent of gene expression. In second part of the dissertation, insulin, a protein, was modified with new photolabile groups and then crosslinked to a solid matrix to create an insoluble photoactivable depot (PAD). Insulin with various degrees of photolabile modifications were purified and studied for their photokinetics. Furthermore, using this new approach, the release of protein from a matrix system was precisely controlled using light. This new photoactivable insulin depot could load several weeks worth of insulin in the volume of a single injection. Therefore, this could potentially solve the problem of multiple insulin injections, administered by millions of diabetics everyday. Furthermore, the amount of insulin released from the depot can be tightly controlled using light. In future, this technique can potentially be coupled with non-invasive continuous glucose monitoring devices for automatic detection and control of blood sugar level in patients. Finally, this PAD approach could be applied to other macromolecules, hormones and drugs. Furthermore, we utilized a universal photolabile crosslinking reagent, developed for insulin, for site-specific end labeling of different types of nucleic acids with these groups. Using these groups, we can temporarily attach other molecules like fluorophore, intercalator, drugs, proteins, etc. on to nucleic acids. Finally, these groups can be photocleaved to regenerate the native nucleic acids. Advisors/Committee Members: Friedman, Simon H. (Simon Hilary), 1966- (advisor).

Subjects/Keywords: Insulin; Labeling; Light

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APA (6^th Edition):

Jain, Piyush K., 1. (2013). Light-activated biomacromolecules . (Thesis). University of Missouri – Kansas City. Retrieved from http://hdl.handle.net/10355/45499

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jain, Piyush K., 1985-. “Light-activated biomacromolecules .” 2013. Thesis, University of Missouri – Kansas City. Accessed February 19, 2020. http://hdl.handle.net/10355/45499.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jain, Piyush K., 1985-. “Light-activated biomacromolecules .” 2013. Web. 19 Feb 2020.

Vancouver:

Jain, Piyush K. 1. Light-activated biomacromolecules . [Internet] [Thesis]. University of Missouri – Kansas City; 2013. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10355/45499.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jain, Piyush K. 1. Light-activated biomacromolecules . [Thesis]. University of Missouri – Kansas City; 2013. Available from: http://hdl.handle.net/10355/45499

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Tasmania

23. St-Pierre, P. Role of the microvasculature in the development of muscle insulin resistance.

Degree: 2010, University of Tasmania

URL: https://eprints.utas.edu.au/22258/1/whole_St-PierrePhilippe2010_thesis.pdf

► Type 2 diabetes is a disease characterised by a decrease in the sensitivity to insulin. Recently evidence has suggested an involvement of the microvasculature in… (more)

▼ Type 2 diabetes is a disease characterised by a decrease in the sensitivity to insulin. Recently evidence has suggested an involvement of the microvasculature in the development of type 2 diabetes. Microvascular perfusion is increased by insulin and impairment of this response may contribute to muscle insulin resistance by limiting insulin and glucose delivery to skeletal muscle myocytes. This thesis focuses on the involvement of the microvascular perfusion in the development of insulin resistance. Two different models were used to assess the impact of the microvascular perfusion on the insulin-mediated glucose disposal. Firstly, 4 weeks of high-fat diet (HFD model) feeding to rats was used as a pre-diabetic model of insulin resistance. Secondly, partial blockage of skeletal muscle microvascular beds with 15 μm diameter latex microspheres (MS model) was used to assess the effect of decreased muscle microvascular perfusion on insulin sensitivity. In each model, insulin sensitivity was determined during hyperinsulinaemic isoglycaemic clamps in anaesthetized rats. Femoral arterial blood flow (FBF) and microvascular perfusion (assessed by the hindleg metabolism of infused 1-methylxanthine) were measured. Hindleg glucose uptake was determined from arteriovenous difference and FBF and muscle glucose uptake from [(¹⁴)C]-2-deoxyglucose uptake. Insulin-mediated increases in femoral blood flow and glucose uptake were blunted in the HFD rats compared to those on the normal diet, while insulininduced microvascular perfusion was completely abolished. To see whether contraction responses were intact on the HFD, the functional response to electrical stimulation in the HFD rats was explored. The contraction-mediated increase in microvascular perfusion and glucose uptake was unaffected by the HFD. In the MS model, microsphere occlusion of hindleg muscle microvasculature diminished microvascular perfusion as well as insulin-mediated glucose uptake, thus causing a vascular-derived acute state of insulin resistance. Next, the long-term effect of microsphere occlusion was assessed. Surprisingly, insulin responses following chronic microsphere occlusion were restored by 2 weeks of recovery post-injection. This may be explained by a rapid angiogenic response in occluded muscle vasculature. Collectively, this thesis demonstrates two key findings that highlight the potential role of the microvasculature in the development of skeletal muscle insulin resistance: (i) that insulin- but not contraction-mediated microvascular responses are impaired in a pre-diabetic model of insulin resistance, and (ii) that acute physical reduction of microvascular flow impairs muscle insulin sensitivity. This furthers our understanding of the aetiology of type 2 diabetes and emphasizes the microvasculature as an interesting therapeutic target for the management of type 2 diabetes.

Subjects/Keywords: Insulin resistance; Diabetes

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APA (6^th Edition):

St-Pierre, P. (2010). Role of the microvasculature in the development of muscle insulin resistance. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/22258/1/whole_St-PierrePhilippe2010_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

St-Pierre, P. “Role of the microvasculature in the development of muscle insulin resistance.” 2010. Thesis, University of Tasmania. Accessed February 19, 2020. https://eprints.utas.edu.au/22258/1/whole_St-PierrePhilippe2010_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

St-Pierre, P. “Role of the microvasculature in the development of muscle insulin resistance.” 2010. Web. 19 Feb 2020.

Vancouver:

St-Pierre P. Role of the microvasculature in the development of muscle insulin resistance. [Internet] [Thesis]. University of Tasmania; 2010. [cited 2020 Feb 19]. Available from: https://eprints.utas.edu.au/22258/1/whole_St-PierrePhilippe2010_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

St-Pierre P. Role of the microvasculature in the development of muscle insulin resistance. [Thesis]. University of Tasmania; 2010. Available from: https://eprints.utas.edu.au/22258/1/whole_St-PierrePhilippe2010_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New South Wales

24. Chen, Daniel. Insulin-sensitive Obesity.

Degree: Clinical School - St Vincent's Hospital, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true

► Introduction: While insulin resistance and obesity coexist, some obese individuals remain insulin-sensitive. We examined phenotypic and metabolic factors associated with insulin sensitivity in both muscle… (more)

▼ Introduction: While insulin resistance and obesity coexist, some obese individuals remain insulin-sensitive. We examined phenotypic and metabolic factors associated with insulin sensitivity in both muscle and liver in obese individuals. Methods: Sixty-four non-diabetic obese adults (29 males) underwent hyperinsulinaemic (15 and 80 mU/m2/min)-euglycaemic clamps with deuterated glucose. Top tertile subjects for glucose infusion rate during the high-dose insulin clamp (GIRHI) were assigned Musclesen and those in the lower two tertiles were assigned Muscleres. Secondarily, top tertile subjects for endogenous glucose production (EGP) suppression during the low-dose insulin clamp were deemed Liversen and the remainder Liverres. Clinical and laboratory parameters, muscle sympathetic nervous activity (MSNA) and visceral, subcutaneous, liver and pancreatic fat were compared.Results: Musclesen and Muscleres had similar body mass index and total fat (P ≥ 0.12), but Musclesen had lower HbA1c (P < 0.001) and systolic (P = 0.01) and diastolic (P = 0.03) blood pressure (BP). Despite similar subcutaneous fat (P = 0.83), Musclesen had lower visceral (P < 0.001) and liver (P < 0.001) fat. Liversen had lower visceral (P < 0.01) and liver (P < 0.01) fat and CRP (P=0.02) than Liverres. When subjects were grouped by both GIRHI and EGP suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin-resistant at both sites. HDL-cholesterol, 1-hour glucose, systolic BP and triglycerides explained 54% of the variance in muscle insulin sensitivity. In men (but not women), MSNA burst frequency correlated inversely with liver insulin sensitivity (r = -0.53, P = 0.02) and positively with the C-reactive protein (CRP) and fibroblast growth factor (FGF)-19 (r = 0.57, P = 0.006 and r = -0.47, P = 0.03, respectively). Conclusions: Obese subjects who were insulin-sensitive at muscle and/or liver exhibited favourable metabolic features, including lower BP, liver and visceral adiposity. Basal sympathetic nerve activity related to liver insulin sensitivity in men, but not in women. MSNA associated with the circulating hepatokines CRP and FGF-19, suggesting a potential hepato-endocrine-autonomic axis. This study identifies factors associated with, and possibly contributing to, insulin sensitivity in obesity. Advisors/Committee Members: Greenfield, Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Chisholm, Don, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: Obesity; Insulin sensitivity

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APA (6^th Edition):

Chen, D. (2015). Insulin-sensitive Obesity. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Chen, Daniel. “Insulin-sensitive Obesity.” 2015. Doctoral Dissertation, University of New South Wales. Accessed February 19, 2020. http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Chen, Daniel. “Insulin-sensitive Obesity.” 2015. Web. 19 Feb 2020.

Vancouver:

Chen D. Insulin-sensitive Obesity. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2020 Feb 19]. Available from: http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true.

Council of Science Editors:

Chen D. Insulin-sensitive Obesity. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true

University of Tasmania

25. Wallis, Michelle G.(Michelle Gaye). Interaction between the vascular and metabolic actions of insulin.

Degree: 2002, University of Tasmania

URL: https://eprints.utas.edu.au/22080/1/whole_WallisMichelleGaye2002_thesis.pdf

Subjects/Keywords: Insulin resistance; Insulin; Insulin

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APA (6^th Edition):

Wallis, M. G. (. G. (2002). Interaction between the vascular and metabolic actions of insulin. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/22080/1/whole_WallisMichelleGaye2002_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wallis, Michelle G (Michelle Gaye). “Interaction between the vascular and metabolic actions of insulin.” 2002. Thesis, University of Tasmania. Accessed February 19, 2020. https://eprints.utas.edu.au/22080/1/whole_WallisMichelleGaye2002_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wallis, Michelle G (Michelle Gaye). “Interaction between the vascular and metabolic actions of insulin.” 2002. Web. 19 Feb 2020.

Vancouver:

Wallis MG(G. Interaction between the vascular and metabolic actions of insulin. [Internet] [Thesis]. University of Tasmania; 2002. [cited 2020 Feb 19]. Available from: https://eprints.utas.edu.au/22080/1/whole_WallisMichelleGaye2002_thesis.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wallis MG(G. Interaction between the vascular and metabolic actions of insulin. [Thesis]. University of Tasmania; 2002. Available from: https://eprints.utas.edu.au/22080/1/whole_WallisMichelleGaye2002_thesis.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Georgia State University

26. Kloc, Noreen. Insulin Dynamic Measures and Weight Change.

Degree: MPH, Public Health, 2016, Georgia State University

URL: https://scholarworks.gsu.edu/iph_theses/437

► ABSTRACT Insulin Dynamic Measures and Weight Change By Noreen Kloc B.S. Computer Information Technology, Purdue University December 7, 2015 INTRODUCTION: Weight gain and obesity… (more)

▼ ABSTRACT Insulin Dynamic Measures and Weight Change By Noreen Kloc B.S. Computer Information Technology, Purdue University December 7, 2015 INTRODUCTION: Weight gain and obesity are risk factors for insulin resistance that can lead to type 2 diabetes and cardiovascular disease; however, there is a complicated interplay between insulin sensitivity (SI), fasting insulin, acute insulin response (AIR), and disposition index (DI) and the relationship of these dynamic measures with weight change is not well understood. AIM: The aim of this study was to investigate the relationships between insulin dynamic measures, SI, fasting insulin, AIR, and DI, with weight change during a 5-years follow-up period in the multi-ethnic cohort of the Insulin Resistance Atherosclerosis Study (IRAS). METHODS: Data on 879 men and women of Hispanic, non-Hispanic White, and African-American race/ethnicity aged 40-69 years were obtained at baseline (1992-1994) and at 5 year follow-up. Crude associations between the insulin dynamic measures and weight change were evaluated using Kruskal-Wallis test and the relationships between log-transformed insulin-related variables were examined using Spearman rank-order analysis. Multivariate regression models evaluated associations of interest adjusted for age, sex, ethnicity, and diabetes status in a time-dependent manner using mixed models. RESULTS: Insulin sensitivity SI inversely coevolves with weight, i.e. greater weight is predicted by lower SI at any time point. To answer the question whether SI is the cause or a consequence of weight change, we examined the associations with the baseline values and a change in SI. In this model, both the baseline SI and change in SI were inversely correlated with weight gain. A similar approach showed that baseline values and change in fasting insulin were directly associated with weight gain. Weight change over time was associated with AIR, i.e. increases in AIR and greater AIR at baseline predicted weight gain. We did not find strong relationships between DI and weight change. DISCUSSION: These results suggest that insulin sensitivity and insulin secretion can modulate weight in a non-diabetic population. Advisors/Committee Members: Dora Il'yasova, PhD, Ruiyan Luo, PhD.

Subjects/Keywords: insulin resistance; insulin sensitivity; insulin secretion; weight; metabolic syndrome; diabetes

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APA (6^th Edition):

Kloc, N. (2016). Insulin Dynamic Measures and Weight Change. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/iph_theses/437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kloc, Noreen. “Insulin Dynamic Measures and Weight Change.” 2016. Thesis, Georgia State University. Accessed February 19, 2020. https://scholarworks.gsu.edu/iph_theses/437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kloc, Noreen. “Insulin Dynamic Measures and Weight Change.” 2016. Web. 19 Feb 2020.

Vancouver:

Kloc N. Insulin Dynamic Measures and Weight Change. [Internet] [Thesis]. Georgia State University; 2016. [cited 2020 Feb 19]. Available from: https://scholarworks.gsu.edu/iph_theses/437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kloc N. Insulin Dynamic Measures and Weight Change. [Thesis]. Georgia State University; 2016. Available from: https://scholarworks.gsu.edu/iph_theses/437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toledo Health Science Campus

27. Bowman, Thomas A. Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome.

Degree: PhD, College of Medicine, 2010, University of Toledo Health Science Campus

URL: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149

► Impaired hepatic insulin clearance causes hyperinsulinemia and secondary insulin resistance, which may progress to involve various components of metabolic syndrome. The carcinoembryonic-related cell adhesion molecule… (more)

▼ Impaired hepatic insulin clearance causes hyperinsulinemia and secondary insulin resistance, which may progress to involve various components of metabolic syndrome. The carcinoembryonic-related cell adhesion molecule 1 (CEACAM1) has been shown to promote insulin clearance, downregulate the mitogenic action of insulin, and limit lipogenesis in the early hours of refeeding. Mice with liver-specific Ceacam1 inactivation (L-SACC1) or with global null mutation (Cc1–/–), exhibit impairment of insulin clearance and hyperinsulinemia, which causes insulin resistance. Since the lack of CEACAM1 correlates with insulin resistance, and regulates insulin action in liver, an important diet-responsive organ, we proposed that reduction of CEACAM1 is implicated in the pathogenesis of diet-induced insulin resistance; and that increasing hepatic levels of CEACAM1 would be protective against metabolic abnormalities associated with metabolic syndrome. Therefore we examined CEACAM1 levels in an animal model of metabolic syndrome and non-alcoholic steatohepatitis (NASH), the low aerobic capacity runner (LCR) rats, in comparison to high aerobic capacity runner (HCR) rats. We found that in response to caloric restriction by 30% over a period of 2-3 months profound improvements in insulin sensitivity and reversal of hepatic inflammation, oxidative stress and fibrosis. Caloric restriction exerts these effects along with increases in fasting levels of CEACAM1 in liver. Additionally we examined the effect of high-fat diet on wild-type mice and on a transgenic mouse with liver-specific overexpression of rat CEACAM1 (L-CC1). We found that an early event associated with high-fat feeding is repression of CEACAM1 by a PPARalpha-mediated mechanism, and that this leads to impaired insulin clearance prior to the development of a pro-inflammatory state. Transgenic overexpression of CEACAM1 in liver prevents hyperinsulinemia and insulin resistance, and limits visceral obesity and the metabolic response to high-fat intake. Advisors/Committee Members: Najjar, Sonia (Committee Chair).

Subjects/Keywords: Biomedical Research; Molecular Biology; CEACAM1; insulin; Hepatic; insulin resistance; PPAR¿¿¿¿; hyperinsulinemia; insulin clearance

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APA (6^th Edition):

Bowman, T. A. (2010). Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149

Chicago Manual of Style (16^th Edition):

Bowman, Thomas A. “Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome.” 2010. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed February 19, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149.

MLA Handbook (7^th Edition):

Bowman, Thomas A. “Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome.” 2010. Web. 19 Feb 2020.

Vancouver:

Bowman TA. Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2010. [cited 2020 Feb 19]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149.

Council of Science Editors:

Bowman TA. Hepatic CEACAM1 Protects Against Metabolic Abnormalities Associated with Metabolic Syndrome. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1271358149

Dalhousie University

28. Nelson, Stephanie. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.

Degree: MS, Department of Physiology & Biophysics, 2010, Dalhousie University

URL: http://hdl.handle.net/10222/13014

► Proghrelin produces three proghrelin derived peptides (PGDP) known for their roles in glucose homeostasis: acylated ghrelin (AG), unacylated ghrelin (UAG), and obestatin (Ob). Only the… (more)

Subjects/Keywords: Ghrelin; Diabetes; insulin; obestatin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nelson, S. (2010). Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/13014

Chicago Manual of Style (16^th Edition):

Nelson, Stephanie. “Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.” 2010. Masters Thesis, Dalhousie University. Accessed February 19, 2020. http://hdl.handle.net/10222/13014.

MLA Handbook (7^th Edition):

Nelson, Stephanie. “Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.” 2010. Web. 19 Feb 2020.

Vancouver:

Nelson S. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. [Internet] [Masters thesis]. Dalhousie University; 2010. [cited 2020 Feb 19]. Available from: http://hdl.handle.net/10222/13014.

Council of Science Editors:

Nelson S. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. [Masters Thesis]. Dalhousie University; 2010. Available from: http://hdl.handle.net/10222/13014

University of Utah

29. Taylor, Joseph Charles. Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;.

Degree: PhD, Biochemistry;, 1973, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1546/rec/1132

► The relationship of fibrinolytic activity produced by baby hamster kidney (BHK-21) cells to surface properties and growth of the cells has been studied. Hydrolysis of… (more)

▼ The relationship of fibrinolytic activity produced by baby hamster kidney (BHK-21) cells to surface properties and growth of the cells has been studied. Hydrolysis of fibrin clots and casein was used to detect cellular protease activity. Cloned, high passage sublines of the BHK-21/C13 cell line were found to produce increased fibrinolysis when compared to low passage BHK-21/C13 cells (C13). Low passage C13 cells were also found to produce an inhibitor of the cellular fibrinolysin. This inhibitory activity was detected when low and high protease-producing cell lines were co-cultivated and could be removed from the C13 cells by trypsin treatment. Inhibitor could again be detected in C13 cell cultures after 6-8.5 hours incubation at 37°C following typsinization. This substance was not detected in supernatant fluids from growing C13 cells and its production was inhibited by incubation of cells at 4°C. All high protease-producing cultures formed colonies in agar suspension, exhibited quantitative increases in agglutinability by concanavalin A (Con A) when compared to low passage cell cultures and grew faster as judged by transfer behavior of cells and increased rates of accumulation of cells in metaphase when grown in the presence of mitotic inhibitor. Low protease-producing C13 cells and sublines low in protease activity isolated from high passage cultures did not grow in agar suspension, exhibited slower growth rates and decreased agglutinability by Con A. Low protease-producing C13 cells could be stimulated to produce increase amounts of fibrinolytic activity with accompanying changes in surface properties characteristic of transformed cells by addition of purines such as hypoxanthine or adenosine to culture media. The effect was reversed by deletion of the purines. Growth of C13 cell in agar suspension did not occur with purine supplementation alone. With the addition of hypoxanthine and thymidine or adenosine and thymidine or adenosine and thymidine, C13 cells formed colonies in agar suspension which were similar to those formed by high protease-producing cell lines. Fibrinolytic activity could be detected from the colonies formed by C13 cells in agar suspension. Treatment of C13 cells suspended in agar with trypsin or fibrinolytically active culture fluids from high protease-producing cells did not result in the multiplication of the cells in agar. Temperature sensitive BHK-21 cells were isolated which were defective for cytokinesis but not karyokinesis. At 39-40°C these cells became enlarged and multinucleated. The defect did not appear to be associated with the cellular fibrinolysin because protease activity could be detected at the permissive and non-permissive temperatures. Growth of temperature sensitive cells in agar suspension did not occur at 39-40°C but cell enlargement, vacillation and lysis were observed in a large portion of the cell population. The data demonstrate that growth in agar suspension, increased Con A agglutinability and increased growth rates are positively associated in some way with the…

Subjects/Keywords: Insulin; Proteins

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Taylor, J. C. (1973). Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1546/rec/1132

Chicago Manual of Style (16^th Edition):

Taylor, Joseph Charles. “Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;.” 1973. Doctoral Dissertation, University of Utah. Accessed February 19, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1546/rec/1132.

MLA Handbook (7^th Edition):

Taylor, Joseph Charles. “Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;.” 1973. Web. 19 Feb 2020.

Vancouver:

Taylor JC. Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;. [Internet] [Doctoral dissertation]. University of Utah; 1973. [cited 2020 Feb 19]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1546/rec/1132.

Council of Science Editors:

Taylor JC. Relationship of fibrinolytic activity to the growth of baby hamster kidney cells in vitro;. [Doctoral Dissertation]. University of Utah; 1973. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1546/rec/1132

University of Georgia

30. Skinner, Kristie Anne. Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women.

Degree: MA, Exercise Science, 2001, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/skinner_kristie_a_200108_ma

► This study was designed to determine whether there was a cumulative effect on several days of acute resistance exercise performed in one week on glucose… (more)

Subjects/Keywords: Insulin resistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Skinner, K. A. (2001). Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women. (Masters Thesis). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/skinner_kristie_a_200108_ma

Chicago Manual of Style (16^th Edition):

Skinner, Kristie Anne. “Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women.” 2001. Masters Thesis, University of Georgia. Accessed February 19, 2020. http://purl.galileo.usg.edu/uga_etd/skinner_kristie_a_200108_ma.

MLA Handbook (7^th Edition):

Skinner, Kristie Anne. “Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women.” 2001. Web. 19 Feb 2020.

Vancouver:

Skinner KA. Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women. [Internet] [Masters thesis]. University of Georgia; 2001. [cited 2020 Feb 19]. Available from: http://purl.galileo.usg.edu/uga_etd/skinner_kristie_a_200108_ma.

Council of Science Editors:

Skinner KA. Effect of three days of acute resistance exercise on insulin and glucose responses in older men and women. [Masters Thesis]. University of Georgia; 2001. Available from: http://purl.galileo.usg.edu/uga_etd/skinner_kristie_a_200108_ma

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