+publisher:"Virginia Tech" +contributor:("Jiang, Honglin")

Virginia Tech

1. Reinholt, Brad Michael. Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice.

Degree: MSin Life Sciences, Animal and Poultry Sciences, 2012, Virginia Tech

► The Src homology 3 domain (SH3) and cysteine rich domain (C1) 3 (Stac3) gene is a novel gene copiously expressed in skeletal muscle. The objective… (more)

Subjects/Keywords: SH3 domain; C1 domain; myogenesis; SH3 and cysteine rich domain 3 (Stac3)

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APA (6^th Edition):

Reinholt, B. M. (2012). Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/76784

Chicago Manual of Style (16^th Edition):

Reinholt, Brad Michael. “Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice.” 2012. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/76784.

MLA Handbook (7^th Edition):

Reinholt, Brad Michael. “Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice.” 2012. Web. 03 Mar 2021.

Vancouver:

Reinholt BM. Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/76784.

Council of Science Editors:

Reinholt BM. Inactivation of Stac3 causes skeletal muscle defects and perinatal death in mice. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/76784

Virginia Tech

2. Zwarycz, Bailey. Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken.

Degree: MS, Animal and Poultry Sciences, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/43761

► PepT1, PepT2 and PHT1 are all members of the proton-coupled oligopeptide transporter family, which are important in the transport of amino acids in peptide form.… (more)

Subjects/Keywords: PHT1; peptide; chicken; transporters; PepT1; PepT2

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APA (6^th Edition):

Zwarycz, B. (2012). Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/43761

Chicago Manual of Style (16^th Edition):

Zwarycz, Bailey. “Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken.” 2012. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/43761.

MLA Handbook (7^th Edition):

Zwarycz, Bailey. “Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken.” 2012. Web. 03 Mar 2021.

Vancouver:

Zwarycz B. Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/43761.

Council of Science Editors:

Zwarycz B. Tissue- and Development-specific Expression of Proton-mediated Peptide Transporters in the Developing Chicken. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/43761

Virginia Tech

3. Jia, Dan. Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment.

Degree: MS, Animal and Poultry Sciences, 2013, Virginia Tech

URL: http://hdl.handle.net/10919/23924

► Growth hormone (GH) has growth-stimulating effects on skeletal muscle and liver but a growth-inhibitory effect on adipose tissue. The mechanisms underlying these actions of GH… (more)

Subjects/Keywords: growth hormone; mouse; C3H10T1/2 cells; liver; myogenesis; adipogenesis

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APA (6^th Edition):

Jia, D. (2013). Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/23924

Chicago Manual of Style (16^th Edition):

Jia, Dan. “Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment.” 2013. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/23924.

MLA Handbook (7^th Edition):

Jia, Dan. “Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment.” 2013. Web. 03 Mar 2021.

Vancouver:

Jia D. Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/23924.

Council of Science Editors:

Jia D. Roles of growth hormone in liver growth and mesenchymal stem cell myogenic and adipogenic lineage commitment. [Masters Thesis]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/23924

Virginia Tech

4. Zhang, Yafei. Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells.

Degree: MS, Animal and Poultry Sciences, 2013, Virginia Tech

URL: http://hdl.handle.net/10919/76864

► The STAC3 gene is a functionally undefined gene predicted to encode a protein containing two SH3 domains and one cysteine-rich domain. In this study, we… (more)

Subjects/Keywords: satellite cells; cattle; skeletal muscle; AP1?1; glucose uptake

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APA (6^th Edition):

Zhang, Y. (2013). Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/76864

Chicago Manual of Style (16^th Edition):

Zhang, Yafei. “Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells.” 2013. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/76864.

MLA Handbook (7^th Edition):

Zhang, Yafei. “Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells.” 2013. Web. 03 Mar 2021.

Vancouver:

Zhang Y. Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/76864.

Council of Science Editors:

Zhang Y. Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells. [Masters Thesis]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/76864

5. Hou, Yuguo. Roles of cholesterol in the proliferation and differentiation of bovine myoblasts.

Degree: MS, Animal and Poultry Sciences, 2017, Virginia Tech

URL: http://hdl.handle.net/10919/87466

► The objective of this study was to assess the potential role of extracellular, cytosolic, and membrane cholesterol in the proliferation and differentiation of bovine myoblasts.… (more)

Subjects/Keywords: cattle; myoblasts; cholesterol; proliferation; differentiation

…at the Virginia Tech Meat Science Center or a local slaughter house and transported to the…

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APA (6^th Edition):

Hou, Y. (2017). Roles of cholesterol in the proliferation and differentiation of bovine myoblasts. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/87466

Chicago Manual of Style (16^th Edition):

Hou, Yuguo. “Roles of cholesterol in the proliferation and differentiation of bovine myoblasts.” 2017. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/87466.

MLA Handbook (7^th Edition):

Hou, Yuguo. “Roles of cholesterol in the proliferation and differentiation of bovine myoblasts.” 2017. Web. 03 Mar 2021.

Vancouver:

Hou Y. Roles of cholesterol in the proliferation and differentiation of bovine myoblasts. [Internet] [Masters thesis]. Virginia Tech; 2017. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/87466.

Council of Science Editors:

Hou Y. Roles of cholesterol in the proliferation and differentiation of bovine myoblasts. [Masters Thesis]. Virginia Tech; 2017. Available from: http://hdl.handle.net/10919/87466

Virginia Tech

6. Ceh, Carrie Ann. Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves.

Degree: MSin Life Sciences, Dairy Science, 2019, Virginia Tech

URL: http://hdl.handle.net/10919/91447

► Dairy calves are born with an under-developed stomach. The stomach has four compartments: the rumen, reticulum, omasum, and abomasum. The rumen is the largest component… (more)

▼ Dairy calves are born with an under-developed stomach. The stomach has four compartments: the rumen, reticulum, omasum, and abomasum. The rumen is the largest component where finger-like projections called papillae grow to absorb nutrients for the calf. It is vital to the calf that the rumen develops not only the papillae to absorb nutrients but also to foster a microbe-rich environment so the microbes can act as a defense mechanism for the calf to aid in fighting disease. While it is known that things like solid feed support the development of the rumen, the mechanism behind how that is happening still remains unclear in the literature. The objective of this study was first to better understand the relationships that exist in the literature between dietary, environmental, and ruminal factors, and second to investigate the claim that certain components of the bacteria in the rumen are stimulating rumen development independently and additively with sodium butyrate. In order to investigate the relationships amongst the dietary, environmental, and ruminal parameters, a computer program called R Studio was used to analyze over 30 different models that extracted data from a database that included a collection of 36 studies from the literature. This is also known as a meta-analysis. The associations of interest that we found were: average daily gain (ADG) of the calf was associated with daily forage intake, calves that were weaned, total starter intake, and total MR intake. Feed efficiency of the calf was associated with the weight of the ruminal contents, daily forage, milk replacer (MR), and starter intakes, percent of the diet composed of starter, and total starter intake. Daily forage intake was associated with the percent of the diet that was starter or MR. Daily starter intake was associated with acid detergent fiber in the starter, a pelleted starter (versus a texturized starter), diets including starter and forage (versus a MR only diet), and the percent of the diet that was MR. Daily MR intake was associated with the percentage of the diet that was starter, final body weight (BW), ruminal propionate concentration, and daily starter intake. These relationships emphasized that although dietary and environmental factors are more closely associated with calf performance, ruminal factors such as rumen contents and volatile fatty acid concentrations appear to have additional, additive influences on calf performance. The second part of the study objective was to explore an idea that, to our knowledge, has not been published in the literature. In the second study, 24 dairy calves were challenged with oral doses of a gram-negative bacteria lipopolysaccharide (LPS), and a short-chain fatty acid sodium butyrate. The hypothesis in this study was that the LPS and sodium butyrate would trigger metabolic pathways on the rumen cell membranes to a greater extent together, versus independently, to increase the amount of cells growing. Calves were assigned to one of four treatments: control (CON), butyrate (BUTY), LPS only (LPS-O),… Advisors/Committee Members: Daniels, Kristy M. (committeechair), White, Robin (committee member), Hanigan, Mark Daniel (committee member), Jiang, Honglin (committee member).

Subjects/Keywords: calf; dairy; lipopolysaccharide; meta-analysis; rumen development

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APA (6^th Edition):

Ceh, C. A. (2019). Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/91447

Chicago Manual of Style (16^th Edition):

Ceh, Carrie Ann. “Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves.” 2019. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/91447.

MLA Handbook (7^th Edition):

Ceh, Carrie Ann. “Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves.” 2019. Web. 03 Mar 2021.

Vancouver:

Ceh CA. Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves. [Internet] [Masters thesis]. Virginia Tech; 2019. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/91447.

Council of Science Editors:

Ceh CA. Environmental, Biochemical, and Dietary Factors that Influence Rumen Development in Dairy Calves. [Masters Thesis]. Virginia Tech; 2019. Available from: http://hdl.handle.net/10919/91447

Virginia Tech

7. Xie, Guohao. Metabolic and endocrine adaptations to heat stress in lactating dairy cows.

Degree: PhD, Animal and Poultry Sciences, 2015, Virginia Tech

URL: http://hdl.handle.net/10919/52903

► Heat stress (HS), a stress response in homeotherms mainly due to elevated ambient temperature and failure of effective heat dissipation, causes a substantial negative economic… (more)

▼ Heat stress (HS), a stress response in homeotherms mainly due to elevated ambient temperature and failure of effective heat dissipation, causes a substantial negative economic impact to livestock industry worldwide. Reduced feed intake, a typical phenomenon observed during HS, was thought to be the primary driver for the milk production loss. However, accumulating evidence indicates that HS influences animal metabolism and endocrine profiles independent of reduced feed intake. Previous studies comparing heat-stressed lactating cows with control group pair-fed (PF) to the intake of HS group but housed in thermoneutral conditions, in order to eliminate the confounding factors result from differentiated feed intakes, showed that HS increased circulating insulin and decreased plasma non-esterified fatty acid (NEFA) in lactating cow, the opposite responses typical of PF cohorts. Therefore, the present studies were performed in order to elucidate the mechanism(s) underlying these counterintuitive changes. In response to a glucose tolerance test (GTT), both HS and PF decreased whole body glucose disposal rate, a sign of insulin resistance. Only PF decreased skeletal muscle insulin sensitivity in terms of reduced protein kinase B (PKB/AKT) phosphorylation, a downstream protein of insulin receptor (IR), while HS group maintained similar intact insulin responsiveness in the liver and skeletal muscle as thermoneutral conditions. There was a global reduction in gene expression of the enzymes related to lipid metabolism in adipose tissue of heat-stressed cows. Similarly, β-adrenergic signaling, a major stimulator of lipid mobilization, was suppressed in terms of NEFA release response during a chronic epinephrine challenge in HS group. After the challenge, phosphorylations of cAMP-response element binding protein (CREB) and hormone sensitive lipase, both located downstream of β-adrenergic receptor, were decreased in HS, but not in thermoneutral conditions, another indicator of impaired adrenergic signaling. In contrast, IR and AKT phosphorylation were increased in HS conditions indicating insulin signaling may be elevated during HS in adipose. Collectively, HS reduces lipid mobilization and appears to favor glucose utilization via alterations of lipid metabolism and hormones signaling pathways. These unique alterations in HS might shed some light on developing counter-HS approaches in the future. Advisors/Committee Members: Rhoads, Robert P. (committeechair), Jiang, Honglin (committee member), Gilbert, Elizabeth R. (committee member), Corl, Benjamin A. (committee member).

Subjects/Keywords: Heat stress; metabolism; endocrinology; glucose; lipid; dairy cow

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APA (6^th Edition):

Xie, G. (2015). Metabolic and endocrine adaptations to heat stress in lactating dairy cows. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/52903

Chicago Manual of Style (16^th Edition):

Xie, Guohao. “Metabolic and endocrine adaptations to heat stress in lactating dairy cows.” 2015. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/52903.

MLA Handbook (7^th Edition):

Xie, Guohao. “Metabolic and endocrine adaptations to heat stress in lactating dairy cows.” 2015. Web. 03 Mar 2021.

Vancouver:

Xie G. Metabolic and endocrine adaptations to heat stress in lactating dairy cows. [Internet] [Doctoral dissertation]. Virginia Tech; 2015. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/52903.

Council of Science Editors:

Xie G. Metabolic and endocrine adaptations to heat stress in lactating dairy cows. [Doctoral Dissertation]. Virginia Tech; 2015. Available from: http://hdl.handle.net/10919/52903

Virginia Tech

8. Leng, Xinyan. Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation.

Degree: PhD, Animal and Poultry Sciences, 2018, Virginia Tech

URL: http://hdl.handle.net/10919/82707

► The overall objective of this dissertation project was to identify factors and mechanisms that control bovine myoblast proliferation, differentiation, and fusion. Three studies were conducted… (more)

▼ The overall objective of this dissertation project was to identify factors and mechanisms that control bovine myoblast proliferation, differentiation, and fusion. Three studies were conducted during this project. The objective of the first study was to determine the effect of oxytocin (OXT) on myoblast proliferation, differentiation and fusion. Treating primary bovine myoblasts in culture with 10 nM and 100 nM OXT for 24 h increased their proliferation rate by 7% (P < 0.05) and 10% (P < 0.05), respectively. Treating bovine myoblasts with either concentration of OXT for 48 h had no effect on their differentiation and fusion, as indicated by no changes in mRNA expression of selected myoblast differentiation markers and fusion index. The objective of the second study was to determine the effects of arachidonic acid (AA) and its major metabolites prostaglandin E2 (PGE2), PGF2a, and PGI2 on myoblast proliferation, differentiation and fusion. Treating myoblasts with 10 μM AA, 1 μM PGE2, 1 μM PGF2α, and 1 μM PGI2 for 24 h each increased the number of proliferating cells by 13%, 24%, 16%, and 16%, respectively, compared to the control (P < 0.05). At the same concentrations, AA, PGE2, and PGF2a stimulated myoblast differentiation and PGE2 improved myoblast fusion (P < 0.05). Treating myoblasts with AA and the cyclooxygenase (COX)-1 and COX-2 inhibitor indomethacin or the COX-2-specific inhibitor NS-398 reversed the stimulatory effect of AA on myoblast proliferation (P < 0.05). The objective of the third study was to determine the role of the proteasome in bovine myoblast differentiation and fusion. It was found that the proteasome activity increased (P < 0.05) during myoblast differentiation and fusion. Adding 5 μM lactacystin, a specific inhibitor of the proteasome, to the differentiation medium nearly completely blocked myoblast differentiation and fusion. Inhibitor of DNA-binding 1 (ID1) is known to inhibit myoblast differentiation and to be degraded by the proteasome in some cells. Both ID1 protein and mRNA expression were found to decrease during myoblast differentiation and fusion, and the decrease in ID1 protein but not ID1 mRNA was reversed (P < 0.05) by treating the cells with lactacystin. In summary, this project reveals that OXT and AA are stimulators of bovine myoblast proliferation and that AA is a stimulator of bovine myoblast differentiation. This project also indicates that the proteasome plays a positive role in bovine myoblast differentiation and fusion, and that it does so perhaps by reducing the accumulation of the ID1 protein. Advisors/Committee Members: Jiang, Honglin (committeechair), Rhoads, Robert P. (committee member), Johnson, Sally E. (committee member), Akers, Robert Michael (committee member).

Subjects/Keywords: Bovine; Satellite cell; Skeletal Muscle; Proliferation; Differentiation; Fusion

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APA (6^th Edition):

Leng, X. (2018). Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/82707

Chicago Manual of Style (16^th Edition):

Leng, Xinyan. “Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation.” 2018. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/82707.

MLA Handbook (7^th Edition):

Leng, Xinyan. “Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation.” 2018. Web. 03 Mar 2021.

Vancouver:

Leng X. Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation. [Internet] [Doctoral dissertation]. Virginia Tech; 2018. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/82707.

Council of Science Editors:

Leng X. Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation. [Doctoral Dissertation]. Virginia Tech; 2018. Available from: http://hdl.handle.net/10919/82707

Virginia Tech

9. Zhao, Lidan. Mechanisms of growth hormone inhibition of adipose tissue growth.

Degree: PhD, Animal and Poultry Sciences, 2013, Virginia Tech

URL: http://hdl.handle.net/10919/49588

► Growth hormone (GH) is a poly-peptide hormone produced by the anterior pituitary. Growth hormone not only stimulates body and muscle growth but also inhibits adipose… (more)

▼ Growth hormone (GH) is a poly-peptide hormone produced by the anterior pituitary. Growth hormone not only stimulates body and muscle growth but also inhibits adipose tissue growth. The overall objective of this study was to determine the mechanisms by which GH inhibits adipose tissue growth. Three studies were conducted to achieve this objective. The first study was conducted to determine if GH inhibits fat tissue growth by stimulating lipolysis. In this study, adipose tissue weight and adipocyte size were compared between GH-deficient growth hormone releasing hormone receptor (Ghrhr) homozygous mutant mice (i.e., lit/lit mice), lit/+ mice, and lit/lit mice injected with GH. lit/lit mice had less body weight but more subcutaneous fat and larger adipocytes compared to lit/+ mice at the same ages. GH treatment to lit/lit mice for four weeks partially reversed these differences. These data suggest that GH inhibits adipose tissue growth in mice at least in part by stimulating lipolysis. Additional data from this study suggest that GH indirectly stimulates lipolysis in vivo and this indirect mechanism is independent of " adrenergic receptors in the adipose tissue. The second study was conducted to investigate if GH inhibits fat tissue growth also by inhibiting adipogenesis. In this study, stromal vascular fraction (SVF) cells were isolated from subcutaneous fat of lit/+ and lit/lit mice and were induced to differentiate into adipocytes in vitro. Oil Red O staining and gene expression analysis revealed that the SVF cells from lit/lit mice had greater adipogenic potential than from lit/+ mice. This suggests that GH inhibits adipose tissue growth also through inhibition of adipogenesis. Additional data from this study suggest that GH may inhibit adipogenesis by inhibiting the formation of adipogenic precursor cells in adipose tissue in mice. The third study was conducted to determine the role of the central component of GH receptor signaling, STAT5, in GH inhibition of differentiation of bovine preadipocytes. In this study, preadipocytes were isolated from subcutaneous fat of adult cattle and were induced to differentiate with or without GH. Based on Oil Red O staining, gene expression, glycerol-3-phosphate dehydrogenase (G3PDH) activity and acetate incorporation assays, GH inhibited differentiation of bovine preadipocytes into adipocytes. GH induced phosphorylation of STAT5 in differentiating bovine preadipocytes. Overexpression of constitutively active STAT5 through adenovirus mimicked the effect of GH on differentiation of bovine preadipocytes. These data support a role of STAT5 in mediating the inhibitory effect of GH on differentiation of bovine preadipocytes into adipocytes. Overall, GH inhibits adipose tissue by both stimulating lipolysis and inhibiting adipogenesis; GH stimulates lipolysis through an indirect mechanism that is independent of the " adrenergic receptors; GH inhibits adipogenesis through a direct mechanism that may involve the transcription factor STAT5. Advisors/Committee Members: Jiang, Honglin (committeechair), Akers, Robert Michael (committee member), Corl, Benjamin A. (committee member), Gerrard, David E. (committee member).

Subjects/Keywords: Adipose tissue; Growth hormone; Adipogenesis; Lipolysis

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APA (6^th Edition):

Zhao, L. (2013). Mechanisms of growth hormone inhibition of adipose tissue growth. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/49588

Chicago Manual of Style (16^th Edition):

Zhao, Lidan. “Mechanisms of growth hormone inhibition of adipose tissue growth.” 2013. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/49588.

MLA Handbook (7^th Edition):

Zhao, Lidan. “Mechanisms of growth hormone inhibition of adipose tissue growth.” 2013. Web. 03 Mar 2021.

Vancouver:

Zhao L. Mechanisms of growth hormone inhibition of adipose tissue growth. [Internet] [Doctoral dissertation]. Virginia Tech; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/49588.

Council of Science Editors:

Zhao L. Mechanisms of growth hormone inhibition of adipose tissue growth. [Doctoral Dissertation]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/49588

Virginia Tech

10. Miller, Carin R. Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte.

Degree: PhD, Animal and Poultry Sciences, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/77043

► Amino acids are assimilated by membrane-associated transporters into and out of enterocytes either in their free form or in the form of peptides. The peptide… (more)

▼ Amino acids are assimilated by membrane-associated transporters into and out of enterocytes either in their free form or in the form of peptides. The peptide transporter, PepT1, is thought to be the major facilitator of peptide transport in the enterocyte. It is unknown if the peptide transporters and free amino acid transporters operate in a compensatory fashion to regulate the amino acid balance within the enterocyte. Therefore, the objective was to examine the regulatory balance between PepT1 and other peptide and free amino acid transporters in enterocytes. The Mouse Small Intestinal Epithelial (MSIE) cells are conditionally immortalized. It was found that MSIE cells express BoAT1, CAT1, CAT2, LAT1, y+LAT1, and y+LAT2, but not PepT1, EAAT3, Bo,+AT, or LAT2, making this model similar to the basolateral membrane of enterocytes. Growing MSIE cells at high temperatures did not affect the nutrient transporter gene expression profile of these cells. Thus, the human colon carcinoma (Caco-2) cell line was used as a small intestinal in vitro model for this study. These cells express PepT1, HPT1, PTR3 EAAT1, EAAT3, rBAT, Bo,+AT CAT1, LAT1, y+LAT1, y+LAT2, ABCC3, ABCC4, which increased from D0 to D21 post confluency, indicating cell maturation. In Caco-2 cells, PepT1 gene silencing was induced in Caco-2 cells. Despite an reduction of PepT1 gene (82%, P < 0.05) protein (96%), no significant difference in any peptide (HPT1, PTR3, ABCC3, ABCC4) or free amino acid transporters (EAAT1, EAAT3, rBAT, Bo,+AT, BoAT1, CAT1, CAT2, LAT1, LAT2, y+LAT1, y+LAT2) between Caco-2 cells treated with PepT1 siRNA and Caco-2 cells treated with Control siRNA was observed. These results suggest no compensation at the gene expression level of these transporters in response to a reduction of PepT1. To account for the limitations of an in vitro and PepT1 kockout mouse model, transgenic chicken models were pursued. Potential cPepT1 overexpressing, cPepT1 shRNA or control shRNA expressing G0 chickens were generated by embryo injection of pseudolentiviral particles followed by ex ovo egg culture. Overall, 9 potential G0 cPepT1 overexpressing chickens, 15 potential G0 cPepT1 shRNA expressing chickens, and 4 potential G0 control shRNA expressing chickens were generated. Advisors/Committee Members: Gerrard, David E. (committeechair), Tu, Zhijian Jake (committee member), Huckle, William R. (committee member), Jiang, Honglin (committee member), Dalloul, Rami A. (committee member).

Subjects/Keywords: Amino Acid; RNAi; Transgenic; Chicken; PepT1; Enterocyte

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APA (6^th Edition):

Miller, C. R. (2012). Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/77043

Chicago Manual of Style (16^th Edition):

Miller, Carin R. “Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte.” 2012. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/77043.

MLA Handbook (7^th Edition):

Miller, Carin R. “Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte.” 2012. Web. 03 Mar 2021.

Vancouver:

Miller CR. Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte. [Internet] [Doctoral dissertation]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/77043.

Council of Science Editors:

Miller CR. Regulatory Balance Between the Peptide Trasporter, Pept1, and Amino Acid Transporter Gene Expression in the Enterocyte. [Doctoral Dissertation]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/77043

Virginia Tech

11. Fisher, Kimberly Denise. Dietary manipulation causes childhood obesity-like characteristics in pigs.

Degree: MS, Animal and Poultry Sciences, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/36176

► An animal model to study complications resulting from childhood obesity is lacking. Our objective was to develop a porcine model for studying mechanisms underlying diet-induced… (more)

Subjects/Keywords: hypercholesterolemia; hypoinsulinemia; adiposity; metabolic syndrome; hyperglycemia

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APA (6^th Edition):

Fisher, K. D. (2011). Dietary manipulation causes childhood obesity-like characteristics in pigs. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/36176

Chicago Manual of Style (16^th Edition):

Fisher, Kimberly Denise. “Dietary manipulation causes childhood obesity-like characteristics in pigs.” 2011. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/36176.

MLA Handbook (7^th Edition):

Fisher, Kimberly Denise. “Dietary manipulation causes childhood obesity-like characteristics in pigs.” 2011. Web. 03 Mar 2021.

Vancouver:

Fisher KD. Dietary manipulation causes childhood obesity-like characteristics in pigs. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/36176.

Council of Science Editors:

Fisher KD. Dietary manipulation causes childhood obesity-like characteristics in pigs. [Masters Thesis]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/36176

Virginia Tech

12. Xie, Ming. Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation.

Degree: MS, Animal and Poultry Sciences, 2014, Virginia Tech

URL: http://hdl.handle.net/10919/79562

► Several uterine-derived paracrine factors have been implicated as critical regulators of conceptus development in cattle, but it remains unclear how these factors work together to… (more)

▼ Several uterine-derived paracrine factors have been implicated as critical regulators of conceptus development in cattle, but it remains unclear how these factors work together to establish and maintain pregnancies. The primary objectives of this work were to establish if cooperative interactions between epidermal growth factor (EGF), fibroblast growth factor-2 (FGF2) and insulin-like growth factor-1 (IGF1) promote bovine trophoblast cell proliferation, and to decipher the intracellular signaling mechanisms employed by these growth factors to regulate cell proliferation. Pilot studies established effective concentrations for each growth factor on a bovine trophoblast cell line (CT1). The first set of studies examined how each factor worked individually or in conjunction with each other to impact CT1 proliferation. Mitotic index (percentage of EdU-positive nuclei after a 45 min challenge) was increased (P<0.05) by supplementation with 10 ng/ml EGF, 10 ng/ml FGF2, or 50 ng/ml IGF1 when compared with non-treated controls. In addition, a greater increase (P<0.05) was detected when all three factors were supplemented together. A follow-up study determined that supplementation of any two growth factors could not replicate the cooperative effect noted when all three factors were provided. A second set of studies was undertaken to examine how mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase/AKT (PI3K/AKT) signaling systems mediate the independent and cooperative effects of these paracrine factors. Both EGF and IGF1 transiently activated mitogen-activated protein kinase3/1 (MAPK3/1) in CT1 cells as determined by Western Blot analysis. By contrast, FGF2 did not affect MAPK3/1 phosphorylation status, but increased AKT phosphorylation status. Neither EGF nor IGF1 impacted AKT activity. Supplementation with a pharmacological inhibitor of MAPK3/1 (PD98059) prevented EGF-, IGF1-, and FGF2-dependent increases in CT1 cell proliferation. This inhibitor also completely abolished the increases in cell proliferation observed when all three factors were supplemented together. Supplementation with a pharmacological inhibitor of AKT (Wortmannin) reduced FGF2-stimulated CT1 proliferation, but did not impact EGF- and IGF1 effects. The AKT inhibitor partially attenuated the cooperative effects of all three factors on CT1 cell proliferation. A final study examined how the combination of EGF, FGF2, and IGF1 affect bovine embryo development. In vitro produced bovine blastocysts were cultured either with the combination of growth factors or vehicle only from day 8 to day 12 post-in vitro fertilization (IVF). The combination of EGF, FGF2, and IGF1 increased (P<0.05) the percentage of hatched blastocysts and outgrowth formation versus controls. Increased (P<0.05) diameters were detected in blastocysts treated with the combination of three growth factors on day 12 post-IVF when compared to controls. Treatment with the combination of EGF, FGF2, and also IGF1 increased (P<0.05) the change of diameter from day 8 to 12 post-IVF. In… Advisors/Committee Members: Ealy, Alan D. (committeechair), Jiang, Honglin (committee member), Johnson, Sally E. (committee member), Li, Liwu (committee member).

Subjects/Keywords: trophoblast; proliferation; bovine; growth factor; outgrowth

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APA (6^th Edition):

Xie, M. (2014). Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/79562

Chicago Manual of Style (16^th Edition):

Xie, Ming. “Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation.” 2014. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/79562.

MLA Handbook (7^th Edition):

Xie, Ming. “Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation.” 2014. Web. 03 Mar 2021.

Vancouver:

Xie M. Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation. [Internet] [Masters thesis]. Virginia Tech; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/79562.

Council of Science Editors:

Xie M. Additive effects among uterine paracrine factors in promoting bovine trophoblast cell proliferation. [Masters Thesis]. Virginia Tech; 2014. Available from: http://hdl.handle.net/10919/79562

Virginia Tech

13. Won, Samantha Gwai Lan. Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine.

Degree: MS, Animal and Poultry Sciences, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/34515

► Heat stress (HS) causes significant losses to the U.S. swine industry in several production and health areas including efficient lean tissue accretion. Perturbations in skeletal… (more)

Subjects/Keywords: heat stress; mTOR; metabolism; swine

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APA (6^th Edition):

Won, S. G. L. (2012). Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/34515

Chicago Manual of Style (16^th Edition):

Won, Samantha Gwai Lan. “Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine.” 2012. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/34515.

MLA Handbook (7^th Edition):

Won, Samantha Gwai Lan. “Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine.” 2012. Web. 03 Mar 2021.

Vancouver:

Won SGL. Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/34515.

Council of Science Editors:

Won SGL. Acute and chronic heat stress alters the metabolic profile of skeletal muscle in growing swine. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/34515

Virginia Tech

14. Tucker, Hannah L. The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers.

Degree: MS, Dairy Science, 2013, Virginia Tech

URL: http://hdl.handle.net/10919/23732

► Our purpose was to determine the effects on mammary gland development in prepubertal heifers given the anti-estrogen tamoxifen. Sixteen Holstein calves were randomly assigned to… (more)

Subjects/Keywords: parenchyma; estrogen; myoepithelial; label retaining

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APA (6^th Edition):

Tucker, H. L. (2013). The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/23732

Chicago Manual of Style (16^th Edition):

Tucker, Hannah L. “The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers.” 2013. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/23732.

MLA Handbook (7^th Edition):

Tucker, Hannah L. “The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers.” 2013. Web. 03 Mar 2021.

Vancouver:

Tucker HL. The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers. [Internet] [Masters thesis]. Virginia Tech; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/23732.

Council of Science Editors:

Tucker HL. The Effects of Tamoxifen on Mammary Development in Prepubertal Heifers. [Masters Thesis]. Virginia Tech; 2013. Available from: http://hdl.handle.net/10919/23732

Virginia Tech

15. Cong, Xiaofei. Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction.

Degree: PhD, Animal and Poultry Sciences, 2016, Virginia Tech

URL: http://hdl.handle.net/10919/78432

► The SH3 and cysteine rich domain 3 (Stac3) gene is expressed specifically in skeletal muscle and essential for skeletal muscle contraction and postnatal life in… (more)

▼ The SH3 and cysteine rich domain 3 (Stac3) gene is expressed specifically in skeletal muscle and essential for skeletal muscle contraction and postnatal life in mice. In this dissertation project, I conducted two studies to further understand the role of STAC3 in skeletal muscle development, growth, and contraction. In the first study, I compared the contractile responses of hindlimb muscles of Stac3 knockout and control mice to electrical stimulation, high [K+]-induced membrane depolarization, and caffeine and 4-chloro-m-cresol (4-CMC) activation of ryanodine receptor (RyR). Frequent electrostimulation-, high [K+]-, 4-CMC- and caffeine-induced maximal tensions in Stac3-deleted muscles were approximately 20%, 29%, 58% and 55% of those in control muscles, respectively. 4-CMC- and caffeine-induced increases in intracellular calcium were not different between Stac3-deleted and control myotubes. Myosin-ATPase and NADH-tetrazolium reductase staining as well as gene expression analyses revealed that Stac3-deleted hindlimb muscles contained more slow type-like fibers than control muscles. These data together confirm a role of STAC3 in EC coupling but also suggest that defective EC coupling is only partially responsible for the significantly reduced contractility in Stac3-deleted hindlimb muscles. In the second study, I determined the potential role of STAC3 in postnatal skeletal muscle growth, fiber composition, and contraction by disrupting Stac3 gene expression in postnatal mice through the Flp-FRT and tamoxifen-inducible Cre-loxP systems. Postnatal Stac3 deletion inhibited body and limb muscle mass gains. Histological staining and gene expression analyses revealed that postnatal Stac3 deletion decreased the size of myofibers and increased the percentage of myofibers containing centralized nuclei without affecting the total myofiber number. Postnatal Stac3 deletion decreased limb muscle strength. Postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced maximal force output in limb muscles. Similarly, postnatal Stac3 deletion reduced electrostimulation- but not caffeine-induced calcium release from the sarcoplasmic reticulum. These results demonstrate that STAC3 is important to myofiber hypertrophy, myofiber type composition, contraction, and EC coupling in postnatal skeletal muscle. Advisors/Committee Members: Jiang, Honglin (committeechair), Gerrard, David E. (committee member), Chin, Eva R. (committee member), Grange, Robert W. (committee member), Akers, Robert Michael (committee member).

Subjects/Keywords: Stac3; muscle contraction; EC coupling; muscle fiber type; muscle growth

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APA (6^th Edition):

Cong, X. (2016). Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/78432

Chicago Manual of Style (16^th Edition):

Cong, Xiaofei. “Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction.” 2016. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/78432.

MLA Handbook (7^th Edition):

Cong, Xiaofei. “Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction.” 2016. Web. 03 Mar 2021.

Vancouver:

Cong X. Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction. [Internet] [Doctoral dissertation]. Virginia Tech; 2016. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/78432.

Council of Science Editors:

Cong X. Role of SH3 and Cysteine-Rich Domain 3 (STAC3) in Skeletal Muscle Development, Postnatal Growth and Contraction. [Doctoral Dissertation]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/78432

Virginia Tech

16. Ma, Liying. Regulatory factors of milk fat synthesis in dairy cows.

Degree: PhD, Dairy Science, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/29120

► The objective of these studies was to investigate the milk fat synthesis regulation by transcription factors. In the first study, bovine mammary epithelial (MAC-T) cells… (more)

▼ The objective of these studies was to investigate the milk fat synthesis regulation by transcription factors. In the first study, bovine mammary epithelial (MAC-T) cells were treated with sterol regulatory element binding protein-1 (SREBP-1) specific siRNA. The mRNA and protein expression of SREBP-1 were decreased by more than 90% by siRNA. Fatty acid (FA) synthesis, uptake, and selected lipogenic enzyme expression were reduced in cells treated with SREBP-1 siRNA. Therefore, SREBP-1 plays an important role in integrated regulation of lipid synthesis in MAC-T cells through regulation of key enzymes. In the second study, MAC-T cells treated with hormones or FA were transfected with luciferase reporter constructs containing response elements for SREBP-1, peroxisome proliferator-activated receptor Î³ (PPARÎ³), or liver X receptor (LXR). The activation of PPARÎ³ and SREBP-1 were stimulated by insulin and insulin combined with leptin, respectively. Trans-10, cis-12 conjugated linoleic acid (CLA) inhibited SREBP-1 activation, and this inhibition was not attenuated by insulin and leptin. Neither trans-10 nor cis-12 double bond inhibited SREBP-1 activation. Taken together, trans-10 and cis-12 double bonds need to be conjugated in CLA to reduce SREBP-1 activation and this inhibition cannot be overcome by insulin and leptin combination in MAC-T cells. In the third study, lactating dairy cows were intravenously infused with 0.625 g/h trans-10, cis-12 CLA for 14 h. We confirmed the appearance of trans-10, cis-12 CLA in the milk of CLA treated cows. Milk and component yield were not affected by the CLA treatment. The desaturation of stearic acid was reduced by CLA. The mRNA and protein expression of transcription factors or lipogenic enzymes were not affected by trans-10, cis-12 CLA. DNA-binding activities for PPARÎ³ and LXR and the activation of SREBP-1 to its mature form were not changed by the treatment. The infusion time in this study was probably too short to induce any changes in transcription factors and lipogenic enzymes. We confirmed DNA-binding activities of PPARÎ³ and LXR in bovine mammary gland. Overall, a prominent role for SREBP-1 in mammary epithelial cell lipid synthetic pathways was described and regulation of transcription factor activation by trans-10, cis-12 CLA was specific to SREBP-1. Advisors/Committee Members: Corl, Benjamin A. (committeechair), Akers, Robert Michael (committee member), Jiang, Honglin (committee member), Wong, Eric A. (committee member).

Subjects/Keywords: milk fat depression; SREBP-1; hormone

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APA (6^th Edition):

Ma, L. (2012). Regulatory factors of milk fat synthesis in dairy cows. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/29120

Chicago Manual of Style (16^th Edition):

Ma, Liying. “Regulatory factors of milk fat synthesis in dairy cows.” 2012. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/29120.

MLA Handbook (7^th Edition):

Ma, Liying. “Regulatory factors of milk fat synthesis in dairy cows.” 2012. Web. 03 Mar 2021.

Vancouver:

Ma L. Regulatory factors of milk fat synthesis in dairy cows. [Internet] [Doctoral dissertation]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/29120.

Council of Science Editors:

Ma L. Regulatory factors of milk fat synthesis in dairy cows. [Doctoral Dissertation]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/29120

Virginia Tech

17. van Eyk, Gregory Ryan. Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs.

Degree: MS, Animal and Poultry Sciences, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/32892

► A pig model of childhood obesity was used to study the effects of dietary energy on body adiposity, and blood parameters associated with impaired glucose… (more)

Subjects/Keywords: glucose tolerance test; : whole body composition; obesity; diabetes; metabolic syndrome

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APA (6^th Edition):

van Eyk, G. R. (2012). Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/32892

Chicago Manual of Style (16^th Edition):

van Eyk, Gregory Ryan. “Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs.” 2012. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/32892.

MLA Handbook (7^th Edition):

van Eyk, Gregory Ryan. “Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs.” 2012. Web. 03 Mar 2021.

Vancouver:

van Eyk GR. Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/32892.

Council of Science Editors:

van Eyk GR. Dietary Fat and Sugar Induce Obesity and Impair Glucose Tolerance in Prepubertal Pigs. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/32892

Virginia Tech

18. Luo, Jing. Investigating the potential anti-diabetic effect of sulforaphane.

Degree: MS, Human Nutrition, Foods, and Exercise, 2014, Virginia Tech

URL: http://hdl.handle.net/10919/49264

► Type 2 diabetes (T2D) is a major public health issue worldwide and it currently affects nearly 26 million people in the United States. It is… (more)

Subjects/Keywords: Sulforaphane; Obesity; T2D; Insulin Sensitivity

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APA (6^th Edition):

Luo, J. (2014). Investigating the potential anti-diabetic effect of sulforaphane. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/49264

Chicago Manual of Style (16^th Edition):

Luo, Jing. “Investigating the potential anti-diabetic effect of sulforaphane.” 2014. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/49264.

MLA Handbook (7^th Edition):

Luo, Jing. “Investigating the potential anti-diabetic effect of sulforaphane.” 2014. Web. 03 Mar 2021.

Vancouver:

Luo J. Investigating the potential anti-diabetic effect of sulforaphane. [Internet] [Masters thesis]. Virginia Tech; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/49264.

Council of Science Editors:

Luo J. Investigating the potential anti-diabetic effect of sulforaphane. [Masters Thesis]. Virginia Tech; 2014. Available from: http://hdl.handle.net/10919/49264

Virginia Tech

19. Li, Xiaoxiao. Ranolazine: a Potential Anti-diabetic Drug.

Degree: MS, Human Nutrition, Foods, and Exercise, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/19202

► Diabetes is a life-long chronic disease that affects more than 24 million Americans. Loss of pancreatic beta-cell mass and function is central to the development… (more)

Subjects/Keywords: Ranolazine; Beta-cell; Apoptosis; Proliferation; Diabetes

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APA (6^th Edition):

Li, X. (2012). Ranolazine: a Potential Anti-diabetic Drug. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/19202

Chicago Manual of Style (16^th Edition):

Li, Xiaoxiao. “Ranolazine: a Potential Anti-diabetic Drug.” 2012. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/19202.

MLA Handbook (7^th Edition):

Li, Xiaoxiao. “Ranolazine: a Potential Anti-diabetic Drug.” 2012. Web. 03 Mar 2021.

Vancouver:

Li X. Ranolazine: a Potential Anti-diabetic Drug. [Internet] [Masters thesis]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/19202.

Council of Science Editors:

Li X. Ranolazine: a Potential Anti-diabetic Drug. [Masters Thesis]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/19202

20. Chen, Liang. Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells.

Degree: PhD, Animal Sciences, Dairy, 2016, Virginia Tech

URL: http://hdl.handle.net/10919/73037

► The key transcription factor sterol regulatory element binding protein-1 (SREBP1) plays a central role in milk fat synthesis. SREBP1 stimulates the transcription of genes encoding… (more)

▼ The key transcription factor sterol regulatory element binding protein-1 (SREBP1) plays a central role in milk fat synthesis. SREBP1 stimulates the transcription of genes encoding lipogenic enzymes. The overall objective of these studies was to investigate the mechanisms of SREBP1 regulation by nutrients. In the first study, chromatin immunoprecipitation (ChIP) accompanied with deep-sequencing was employed to investigate the potential sterol regulatory elements (SRE) in the promoter of SREBP1-target genes. The SRE in three known SREBP1-target genes SREBP1, fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD) were first validated in a bovine mammary epithelial cell line (MacT) and in bovine mammary tissues. At least one or two SRE binding sites in 24 selected lipogenic genes were identified within 50,000 base pair to the 5'-transcription start site through ChIP-seq. The genes closest to the highest enriched peaks were involved in cell integrity, defense or signal transduction whereas lipogenic genes were not among the top enrichment leading to the questions about the success of the ChIP. The second study was conducted to determine the effect of t10, c12-conjugated linoleic acid (CLA) on insulin induced gene-1 (Insig1), an endoplasmic reticulum (ER) protein that anchors SREBP1 and prevents proteolytic activation of SREBP1. MacT cells were treated with increasing levels of t10, c12-CLA. High concentration of t10, c12-CLA inhibited Insig1 degradation therefore decreased SREBP1 maturation. Furthermore, immunoprecipitation (IP) confirmed that t10, c12-CLA reduced Insig1 proteasomal iv degradation by disrupting the interaction between Insig1 and UBX domain-containing protein 8 (Ubxd8), which is part of a degradation complex that removes Insig1 from the ER. In the third study, three potential regulators of SREBP1 activation and their pathways were investigated in insulin, t10, c12-CLA or glucose treated MacT cells. Insulin-induced mammalian target of rapamycin (mTOR) signaling stimulated lipogenesis via activation of SREBP1 and the stimulatory effect was based on the regulation on cAMP response element binding protein coactivator 2 (CRTC2) phosphorylation, Lipin1 translocation and glycogen synthase kinase-3 (GSK3)-dependent proteasomal degradation. t10, c12-CLA inhibited SREBP1 through AMP-activated protein kinase (AMPK) phosphorylation, a key protein kinase in energy homeostasis. Glucose stabilized the SREBP1 chaperone protein SCAP and facilitated SREBP1 activation. Overall, SREBP1 activation is under specific regulation of t10, c12-CLA and interacts with multiple major cellular signaling pathways in response to hormonal stimulation and nutrient availability. Advisors/Committee Members: Corl, Benjamin A. (committeechair), Ferreira, Gonzalo (committee member), Jiang, Honglin (committee member), Akers, Robert Michael (committee member).

Subjects/Keywords: SREBP1; t10; c12-CLA; mTOR; Insig1

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

APA (6^th Edition):

Chen, L. (2016). Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/73037

Chicago Manual of Style (16^th Edition):

Chen, Liang. “Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells.” 2016. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/73037.

MLA Handbook (7^th Edition):

Chen, Liang. “Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells.” 2016. Web. 03 Mar 2021.

Vancouver:

Chen L. Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells. [Internet] [Doctoral dissertation]. Virginia Tech; 2016. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/73037.

Council of Science Editors:

Chen L. Regulation of sterol regulatory element binding protein-1 in bovine mammary epithelial cells. [Doctoral Dissertation]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/73037

Virginia Tech

21. Fu, Zhuo. The anti-diabetic mechanisms by isoflavone genistein.

Degree: PhD, Human Nutrition, Foods, and Exercise, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/37816

► Diabetes is growing public health problem in the United States. Both in Type 1 and Type 2 diabetes, the deterioration of glycemic control over time… (more)

▼ Diabetes is growing public health problem in the United States. Both in Type 1 and Type 2 diabetes, the deterioration of glycemic control over time is largely due to insulin secretory dysfunction and significant loss of functional β-cells. As such, the search for novel agents that promote β-cell survival and preserve functional β-cell mass are one of the essential strategies to prevent and treat the onset of diabetes. Genistein, a flavonoid in legumes and some herbal medicines, has various biological actions. It was recently shown that dietary intake of foods containing genistein improves diabetes in both experimental animals and humans. However, the potential anti-diabetic mechanisms of genistein are unclear. In the present study, we first investigated the effect of genistein on β-cell insulin secretion and proliferation and cellular signaling related to these effects in vitro and in vivo. We then determined its anti-diabetic potential in insulin-deficient and obese diabetic mouse models. The results in our study showed that exposure of clonal insulin secreting (INS1E) cells or isolated pancreatic islets to genistein at physiologically relevant concentrations (1-10 μM) enhanced glucose-stimulated insulin secretion (GSIS), whereas insulin content was not altered, suggesting that genistein-enhanced GSIS is not due to a modulation of insulin synthesis. This genistein's effect is protein tyrosine kinase- and KATP channel-independent. In addition, genistein had no effect on glucose transporter-2 expression or cellular ATP production, but similarly augmented pyruvate-stimulated insulin secretion in INS1E cells, indicating that genistein improvement of insulin secretion in β-cells is not related to an alternation in glucose uptake or the glycolytic pathway. Further, genistein (1-10 μM) induced both INS1 and human islet β-cell proliferation following 24 h of incubation, with 5 μM genistein inducing a maximal 27% increase. The effect of genistein on β-cell proliferation was neither dependent on estrogen receptors, nor shared by 17β-estradiol or a host of structurally related flavonoid compounds. Pharmacological or molecular intervention of PKA or ERK1/2 completely abolished genistein-stimulated β-cell proliferation, suggesting that both molecules are essential for genistein action. Consistent with its effect on cell proliferation, genistein induced cAMP/PKA signaling and subsequent phosphorylation of ERK1/2 in both INS1 cells and human islets. Furthermore, genistein induced protein expression of cyclin D1, a major cell-cycle regulator essential for β-cell growth. Dietary intake of genistein significantly improved hyperglycemia, glucose tolerance, and blood insulin levels in both insulin deficient type 1 and obese type 2 diabetic mice, concomitant with improved islet β-cell proliferation, survival, and mass. These changes were not due to alternations in animal body weight gain, food intake, fat deposit, plasma lipid profile, or peripheral insulin sensitivity. Collectively, these findings provide better understanding of the… Advisors/Committee Members: Liu, Dongmin (committeechair), Bassaganya-Riera, Josep (committee member), Jiang, Honglin (committee member), Barbeau, William E. (committee member), Huckle, William R. (committee member).

Subjects/Keywords: apoptosis; proliferation; insulin secretion; Î²-cell; diabetes; genistein

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APA (6^th Edition):

Fu, Z. (2011). The anti-diabetic mechanisms by isoflavone genistein. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/37816

Chicago Manual of Style (16^th Edition):

Fu, Zhuo. “The anti-diabetic mechanisms by isoflavone genistein.” 2011. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/37816.

MLA Handbook (7^th Edition):

Fu, Zhuo. “The anti-diabetic mechanisms by isoflavone genistein.” 2011. Web. 03 Mar 2021.

Vancouver:

Fu Z. The anti-diabetic mechanisms by isoflavone genistein. [Internet] [Doctoral dissertation]. Virginia Tech; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/37816.

Council of Science Editors:

Fu Z. The anti-diabetic mechanisms by isoflavone genistein. [Doctoral Dissertation]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/37816

Virginia Tech

22. Alkhalidy, Hana Awwad. Flavonol kaempferol in the regulation of glucose homeostasis in diabetes.

Degree: PhD, Human Nutrition, Foods, and Exercise, 2016, Virginia Tech

URL: http://hdl.handle.net/10919/82485

► Diabetes mellitus is a major public health concern. Although the accessible novel drugs, techniques, and surgical intervention has improved the survival rate of individuals with… (more)

▼ Diabetes mellitus is a major public health concern. Although the accessible novel drugs, techniques, and surgical intervention has improved the survival rate of individuals with diabetes, the prevalence of diabetes is still rising. Type 2 diabetes (T2D) is a result of chronic insulin resistance (IR) and loss of β-cell mass and function. Therefore, the search for naturally occurring, low-cost, and safe compounds that could enhance insulin sensitivity and protect functional β-cell mass can be an effective strategy to prevent this disease. Kaempferol, a flavonol present in various medicinal herbs and edible plants, has been shown to elicit various pharmacological activities in preclinical studies. However, studies investigating the effect of kaempferol on diabetes are limited. In this dissertation, I explored the anti-diabetic potential of dietary intake of kaempferol in diet-induced obese mice and insulin-deficient diabetic mice. First, kaempferol was supplemented in the diet to determine whether it can prevent IR and hyperglycemia in high fat (HF) diet-induced obese mice or STZ-induced obese diabetic mice. To evaluate its efficacy for treating diabetes, kaempferol was administrated once daily via oral gavage to diet-induced obese and insulin-resistant mice or lean STZ-induced diabetic mice. The results demonstrated that long-term oral administration of kaempferol prevents HFD-induced metabolic disorders in middle-aged obese mice. Oral administration of kaempferol improved glucose intolerance and insulin sensitivity, and this effect was associated with increased Glut4 and AMPKa expression in muscle and adipose tissues. Consistent with our findings from the in iii vitro study in C2C12 muscle cell line, these findings suggest that kaempferol may reduce IR at the molecular level by improving glucose metabolism in peripheral tissues. In the second study, dietary kaempferol supplementation prevented hyperglycemia and glucose intolerance by protecting β-cell against the induced damage in obese STZ-induced diabetic mice. In the third study, the administration of kaempferol by oral gavage significantly ameliorated hyperglycemia and glucose intolerance and reduced the incidence of diabetes from 100 % to 77.8% in lean STZinduced diabetic mice. This kaempferol effect was associated with reduced hepatic glucose production, the primary contributor to hyperglycemia, and increased glucose oxidation in the muscle of diabetic mice. Kaempferol treatment restored hexokinase activity in the liver and skeletal muscle and reduced pyruvate carboxylase (PC) activity and glycogenolysis in the liver. Unlike its effect on T2D mice, kaempferol effect in lean STZ-induced diabetic mice was not associated with changes in plasma insulin levels. In the last study, we found that administration of kaempferol by oral gavage significantly improved blood glucose control by suppressing hepatic glucose production and improving glucose intolerance in obese insulin-resistant mice. Similar to its effect in old obese mice, kaempferol… Advisors/Committee Members: Liu, Dongmin (committeechair), Jiang, Honglin (committee member), Good, Deborah J. (committee member), Hulver, Matthew W. (committee member).

Subjects/Keywords: Kaempferol; diabetes; glucose control; β-cells; insulin resistance; glucose production

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APA (6^th Edition):

Alkhalidy, H. A. (2016). Flavonol kaempferol in the regulation of glucose homeostasis in diabetes. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/82485

Chicago Manual of Style (16^th Edition):

Alkhalidy, Hana Awwad. “Flavonol kaempferol in the regulation of glucose homeostasis in diabetes.” 2016. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/82485.

MLA Handbook (7^th Edition):

Alkhalidy, Hana Awwad. “Flavonol kaempferol in the regulation of glucose homeostasis in diabetes.” 2016. Web. 03 Mar 2021.

Vancouver:

Alkhalidy HA. Flavonol kaempferol in the regulation of glucose homeostasis in diabetes. [Internet] [Doctoral dissertation]. Virginia Tech; 2016. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/82485.

Council of Science Editors:

Alkhalidy HA. Flavonol kaempferol in the regulation of glucose homeostasis in diabetes. [Doctoral Dissertation]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/82485

23. Zhang, Wei. Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals.

Degree: PhD, Animal and Poultry Sciences, 2014, Virginia Tech

URL: http://hdl.handle.net/10919/64416

► Obesity is a physiological consequence of dysregulated energy homeostasis. Energy homeostasis depends on energy intake and energy expenditure. Factors controlling the development of different adipose… (more)

▼ Obesity is a physiological consequence of dysregulated energy homeostasis. Energy homeostasis depends on energy intake and energy expenditure. Factors controlling the development of different adipose tissue deposits in the body and their distinct metabolic phenotypes are of considerable interest from both an agricultural and biomedical perspective. Following the literature review, the first chapter was devoted to studies designed to bridge the neural-adipose interface in understanding the relationship between appetite regulation and adipose tissue deposition in chickens, using chickens selected for low or high juvenile body weight as a model. Appetite regulation in the brain, particularly the hypothalamus, is the main factor governing food intake. Neuropeptide Y (NPY), known as a potent orexigenic factor, also promotes energy storage in fat in mammals and thus has a dual role in promoting energy intake via appetite regulation in the brain and energy storage/expenditure via direct effects on adipose tissue function. There have been no reports of the effects of NPY on adipose tissue function in any avian species. By exposing chicken preadipocytes to different concentration of NPY, we found that NPY enhances both proliferation and differentiation and thus appears to play a major role in chicken adipogenesis, an effect that has not yet been reported, to our knowledge. In the body weight selected chicken lines, we found that NPY and receptor sub-type expression was elevated in the abdominal fat of chickens from the high body weight chicken line and expression of these genes displayed heterosis in the reciprocal crosses of the parental lines as compared to both the high and low body weight selected lines. Intriguingly, expression of those same genes was greater in the low weight than high weight chickens in the hypothalamus. Hypothalamic transcriptomic profiling revealed that genes involved in serotonergic and dopaminergic systems may also play an important role in both appetite regulation and insulin-regulated energy homeostasis in the body weight chicken lines. Intracerebroventricular injection of serotonin in broiler chicks was associated with a dose and time dependent reduction in food intake that was coupled with the activation of the ventromedial hypothalamus and arcuate nucleus, as determined by c-fos immunoreactivity. The remainder of this dissertation project describes the effects of knocking down expression of a recently discovered transcription factor, ZBED6, on mouse preadipocyte proliferation and differentiation. The dissertation ends with a study using diet-induced porcine prepubertal obesity as a model to examine differences in adipokine gene expression between different fat depots from pigs that consumed diets that differed in carbohydrate composition. Overall, we conclude that both NPY and monoamines such as serotonin and dopamine are of importance in the regulation of energy balance in chickens. Moreover, we propose that NPY is a factor that mediates hypothalamus and adipose tissue crosstalk in chickens.… Advisors/Committee Members: Gilbert, Elizabeth R. (committeechair), Jiang, Honglin (committee member), Siegel, Paul B. (committee member), Cline, Mark Andrew (committee member), Liu, Dongmin (committee member), Andersson, Leif (committee member).

Subjects/Keywords: NPY; adipogenesis; body weight lines; appetite regulation; energy homeostasis; serotonin; 3T3L1 cell line; ZBED6; cytokines; inflammation; obesity

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APA (6^th Edition):

Zhang, W. (2014). Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/64416

Chicago Manual of Style (16^th Edition):

Zhang, Wei. “Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals.” 2014. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/64416.

MLA Handbook (7^th Edition):

Zhang, Wei. “Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals.” 2014. Web. 03 Mar 2021.

Vancouver:

Zhang W. Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals. [Internet] [Doctoral dissertation]. Virginia Tech; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/64416.

Council of Science Editors:

Zhang W. Neurological - Molecular Interface in Food Intake and Metabolism in Birds and Mammals. [Doctoral Dissertation]. Virginia Tech; 2014. Available from: http://hdl.handle.net/10919/64416

Virginia Tech

24. Ge, Xiaomei. Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth.

Degree: PhD, Animal and Poultry Sciences, 2012, Virginia Tech

URL: http://hdl.handle.net/10919/77332

► Three studies were conducted to achieve the following respective objectives: 1) to determine the cellular mechanism by which growth hormone (GH) stimulates skeletal muscle growth;… (more)

▼ Three studies were conducted to achieve the following respective objectives: 1) to determine the cellular mechanism by which growth hormone (GH) stimulates skeletal muscle growth; 2) to identify the signaling pathways that mediate the different effects of insulin-like growth factor I (IGF-I) on skeletal muscle growth; and 3) to determine the role of a functionally unknown gene named SH3 and cysteine rich domain 3 (STAC3) in myogenesis. In the first study, the myogenic precursor cells, satellite cells, were isolated from cattle and allowed to proliferate as myoblasts or induced to fuse into myotubes in culture. GH increased protein synthesis without affecting protein degradation in myotubes; GH had no effect on proliferation of myoblasts; GH had no effect on IGF-I mRNA expression in either myoblasts or myotubes. These data suggest that GH stimulates skeletal muscle growth in cattle in part through stimulation of protein synthesis and that this stimulation is not mediated through increased IGF-I mRNA expression in the muscle. In the second study, the signaling pathways mediating the effects of IGF-I on proliferation of bovine myoblasts and protein synthesis and degradation in bovine myotubes were identified by adding to the culture medium rapamycin, LY294002, and PD98059, which are specific inhibitors of the signaling molecules mTOR, AKT, and ERK, respectively. The effectiveness of these inhibitors was confirmed by Western blotting. Proliferation of bovine myoblasts was stimulated by IGF-I, and this stimulation was partially blocked by PD98059 and completely blocked by rapamycin or LY294002. Protein degradation in myotubes was inhibited by IGF-I and this inhibition was completely relieved by LY294002, but not by rapamycin or PD98059. Protein synthesis in myotubes was increased by IGF-I, and this increase was completely blocked by rapamycin, LY294002, or PD98059. These data demonstrate that IGF-I stimulates proliferation of bovine myoblasts and protein synthesis in bovine myotubes through both the PI3K/AKT and the MAPK signaling pathways and that IGF-I inhibits protein degradation in bovine myotubes through the PI3K/AKT pathway only. In the third study, the potential roles of STAC3 in myoblast proliferation, differentiation, and fusion were investigated. Overexpression of STAC3 inhibited differentiation of C2C12 cells (a murine myoblast cell line) and fusion of these cells into myotubes, whereas knockdown of STAC3 had the opposite effects. Either STAC3 overexpression or STAC3 knockdown had no effect on proliferation of C2C12 cells. Myoblasts from STAC3-deficient mouse embryos had a greater ability to fuse into myotubes than control myoblasts; the former cells also expressed more mRNAs for the myogenic regulators MyoD and myogenin and the adult myosin heavy chain protein MyHC1 than the latter. These results suggest that STAC3 inhibits myoblast differentiation and fusion. Advisors/Committee Members: Jiang, Honglin (committeechair), Corl, Benjamin A. (committee member), Escobar, Jeffery E. (committee member), Gerrard, David E. (committee member), Liu, Dongmin (committee member), Wong, Eric A. (committee member).

Subjects/Keywords: Signaling; Differentiation; Myoblasts; Myotubes; Proliferation; Fusion

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APA (6^th Edition):

Ge, X. (2012). Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/77332

Chicago Manual of Style (16^th Edition):

Ge, Xiaomei. “Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth.” 2012. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/77332.

MLA Handbook (7^th Edition):

Ge, Xiaomei. “Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth.” 2012. Web. 03 Mar 2021.

Vancouver:

Ge X. Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth. [Internet] [Doctoral dissertation]. Virginia Tech; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/77332.

Council of Science Editors:

Ge X. Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth. [Doctoral Dissertation]. Virginia Tech; 2012. Available from: http://hdl.handle.net/10919/77332

Virginia Tech

25. Klang, Judith Elisa. Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line.

Degree: MS, Animal and Poultry Sciences, 2002, Virginia Tech

URL: http://hdl.handle.net/10919/30880

► Absorption of dietary proteins can be met through the uptake of free amino acids or as small peptides. A peptide transport protein, PepT1, is responsible… (more)

▼ Absorption of dietary proteins can be met through the uptake of free amino acids or as small peptides. A peptide transport protein, PepT1, is responsible for the absorption of intact peptides arising from digestion of dietary proteins. PepT1 is driven by a H+-coupled transport system that allows for the absorption of small peptides through the intestinal brush border membrane. Screening of a porcine intestinal cDNA library with a sheep PepT1 cDNA probe resulted in the identification of three porcine PepT1 (pPepT1) cDNAs of varying sizes and sequences. Each variant cDNA isolated was cloned into a mammalian expression vector, sequenced, and expressed in Chinese hamster ovary (CHO) cells. Peptide transport was assessed by uptake studies using the radiolabeled dipeptide [3H]-Gly-Sar. Only one of the three cDNAs encoding for a protein of 708 amino acids induced H+-dependent peptide transport activity. Through computer analysis, a putative protein structure for pPepT1 was developed. The transporter has an unusual 13 transmembrane structure with the N-terminus located extracellularly and the C-terminus located intracellularly. Seven glycosylation sites and three protein kinase C phosphorylation sites are located throughout the protein. Expression of pPepT1 activity in CHO cells had a optimal peptide uptake at 18-24 hours. The transporter showed optimal uptake at a pH of 5.5-6.0. Eighteen different unlabeled dipeptides and tripeptides were found to inhibit the uptake of [3H] -Gly-Sar in competition studies. The IC50 of 13 of the dipeptides and two tripeptides ranged between 0.015 to 0.4 mmol/L. The exceptions were Lys-Lys, Arg-Lys, and Lys-Trp-Lys, which showed IC50 values greater than 1.37 mmol/L and appear to be poor substrates for pPepT1. All three of the tetrapeptides examined showed very high IC50 values and inhibition of the uptake of Gly-Sar was too small to measure even at a 10mM concentration. Dipeptides and tripeptides appear to be substrates for the porcine intestinal peptide transporter while tetrapeptides do not appear to be transported. Advisors/Committee Members: Wong, Eric A. (committeechair), Webb, Kenneth E. Jr. (committee member), Jiang, Honglin (committee member).

Subjects/Keywords: Peptide Transport; Pig; PepT1

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APA (6^th Edition):

Klang, J. E. (2002). Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/30880

Chicago Manual of Style (16^th Edition):

Klang, Judith Elisa. “Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line.” 2002. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/30880.

MLA Handbook (7^th Edition):

Klang, Judith Elisa. “Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line.” 2002. Web. 03 Mar 2021.

Vancouver:

Klang JE. Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line. [Internet] [Masters thesis]. Virginia Tech; 2002. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/30880.

Council of Science Editors:

Klang JE. Cloning, Sequencing and Expression of a Porcine Intestinal Peptide Transporter in a Mammalian Cell Line. [Masters Thesis]. Virginia Tech; 2002. Available from: http://hdl.handle.net/10919/30880

Virginia Tech

26. Tian, Xi. An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model.

Degree: MS, Animal and Poultry Sciences, 2008, Virginia Tech

URL: http://hdl.handle.net/10919/36307

► Dilated cardiomyopathy (DCM), a disease of the myocardium, causes morbidity and premature death in humans and other domestic animals including turkeys. Though DCM results from… (more)

Subjects/Keywords: Dilated cardiomyopathy; Turkeys; Mitochondrial DNA; Actin

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APA (6^th Edition):

Tian, X. (2008). An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/36307

Chicago Manual of Style (16^th Edition):

Tian, Xi. “An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model.” 2008. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/36307.

MLA Handbook (7^th Edition):

Tian, Xi. “An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model.” 2008. Web. 03 Mar 2021.

Vancouver:

Tian X. An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model. [Internet] [Masters thesis]. Virginia Tech; 2008. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/36307.

Council of Science Editors:

Tian X. An Assessment of the Molecular Basis of Toxin-induced Dilated Cardiomyopathy in an Avian Animal Model. [Masters Thesis]. Virginia Tech; 2008. Available from: http://hdl.handle.net/10919/36307

Virginia Tech

27. Eleswarapu, Satyanarayana Venkata. Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver.

Degree: MS, Animal and Poultry Sciences, 2004, Virginia Tech

URL: http://hdl.handle.net/10919/42801

► Liver gene expression changes during development and is affected by growth hormone (GH). These changes in gene expression may be due to the differential expression… (more)

Subjects/Keywords: Growth Hormone; Bovine; Liver; Liver-Enriched Transcription Factors

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APA (6^th Edition):

Eleswarapu, S. V. (2004). Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/42801

Chicago Manual of Style (16^th Edition):

Eleswarapu, Satyanarayana Venkata. “Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver.” 2004. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/42801.

MLA Handbook (7^th Edition):

Eleswarapu, Satyanarayana Venkata. “Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver.” 2004. Web. 03 Mar 2021.

Vancouver:

Eleswarapu SV. Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver. [Internet] [Masters thesis]. Virginia Tech; 2004. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/42801.

Council of Science Editors:

Eleswarapu SV. Developmental and Growth Hormone Regulation of the Expression of Liver-Enriched Transcription Factors in Bovine Liver. [Masters Thesis]. Virginia Tech; 2004. Available from: http://hdl.handle.net/10919/42801

Virginia Tech

28. Boorgula, Smitha. Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice.

Degree: MS, Animal and Poultry Sciences, 2007, Virginia Tech

URL: http://hdl.handle.net/10919/32186

► Xenobiotics are plant derived compounds metabolized by phase I and II liver enzymes. Phase I enzymes increase, and phase II enzymes decrease, xenobiotic toxicity. Xenobiotics… (more)

Subjects/Keywords: Ergotamine; Gene expression; Hepatic phase I and II enzymes; Sulforaphane

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APA (6^th Edition):

Boorgula, S. (2007). Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/32186

Chicago Manual of Style (16^th Edition):

Boorgula, Smitha. “Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice.” 2007. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/32186.

MLA Handbook (7^th Edition):

Boorgula, Smitha. “Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice.” 2007. Web. 03 Mar 2021.

Vancouver:

Boorgula S. Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice. [Internet] [Masters thesis]. Virginia Tech; 2007. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/32186.

Council of Science Editors:

Boorgula S. Assessing Hepatic Gene Expression in Response to Xenobiotic Exposure in Mice. [Masters Thesis]. Virginia Tech; 2007. Available from: http://hdl.handle.net/10919/32186

Virginia Tech

29. Van, Ling. Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos.

Degree: MS, Animal and Poultry Sciences, 2002, Virginia Tech

URL: http://hdl.handle.net/10919/9854

► A cDNA clone encoding a turkey intestinal peptide transporter, tPepT1, was isolated from a turkey small intestinal cDNA library by screening with our chicken PepT1… (more)

▼ A cDNA clone encoding a turkey intestinal peptide transporter, tPepT1, was isolated from a turkey small intestinal cDNA library by screening with our chicken PepT1 (cPepT1) cDNA probe. The tPepT1 cDNA is 2,921-bp long and encodes a 79.4 kDa protein of 714 amino acids (AA) with 12 predicted transmembrane domains. The isoelectric point (pI) of tPepT1 is 5.9, which is much lower than that of PepT1 cloned from chicken (pI = 7.5) and other species. The AA sequence of tPepT1 is 94.3% identical to cPepT1 and ~ 60% identical to PepT1 from rat, sheep, rabbit, and human. Using a two-electrode voltage-clamp technique in Xenopus oocytes expressing tPepT1, Gly-Sar transport was pH dependent, but independent of Na+ and K+. For the dipeptides Gly-Sar and Met-Met, the evoked inward currents indicated that the transporter was saturable and had a high affinity for these substrates. However, transport of the tetrapeptide, Met-Gly-Met-Met, exhibited a possible substrate inhibition. To study developmental regulation of PepT1 in broiler and turkey embryos, 12 Nicholas turkey or Cobb x Cobb broiler embryos (six males and six females) were sampled daily from 5 d before hatch to the day of hatch (d 0). The abundance of PepT1 mRNA in the small intestine was quantified densitometrically from northern blots after hybridization with full-length cPepT1 and tPepT1 cDNA as probes. There was a quadratic increase (P < 0.001) in PepT1 mRNA abundance with age in turkey and broiler embryos. The relative increase in abundance of PepT1 mRNA in intestinal tissue from 5 d before hatch to d 0 was much less in the turkey than in the broiler (3.2-fold vs 14-fold). The dramatic increase in PepT1 mRNA abundance indicates a developmental regulation of the PepT1 gene and that there may be a crucial role for PepT1 in the neonatal chick and poult. Advisors/Committee Members: Webb, Kenneth E. Jr. (committeechair), Bloomquist, Jeffrey R. (committee member), Jiang, Honglin (committee member), Wong, Eric A. (committee member).

Subjects/Keywords: Turkey; Embryo; Developmental regulation; Peptide transporter; Broiler

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APA (6^th Edition):

Van, L. (2002). Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/9854

Chicago Manual of Style (16^th Edition):

Van, Ling. “Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos.” 2002. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/9854.

MLA Handbook (7^th Edition):

Van, Ling. “Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos.” 2002. Web. 03 Mar 2021.

Vancouver:

Van L. Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos. [Internet] [Masters thesis]. Virginia Tech; 2002. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/9854.

Council of Science Editors:

Van L. Molecular Cloning and Functional Characterization of a Turkey Intestinal Peptide Transporter (tPepT1), and Developmental Regulation of PepT1 Expression in Turkey and Broiler Embryos. [Masters Thesis]. Virginia Tech; 2002. Available from: http://hdl.handle.net/10919/9854

Virginia Tech

30. Chen, Hong. Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line.

Degree: PhD, Animal and Poultry Sciences, 2001, Virginia Tech

URL: http://hdl.handle.net/10919/29184

► To study peptide absorption in chickens, an intestinal peptide transporter cDNA (cPepT1) was isolated from a chicken cDNA library. The cDNA was 2,914-bp and encoded… (more)

▼ To study peptide absorption in chickens, an intestinal peptide transporter cDNA (cPepT1) was isolated from a chicken cDNA library. The cDNA was 2,914-bp and encoded a protein of 714 amino acid residues. Twenty-three di-, tri-, and tetra-peptides were used for functional analysis of cPepT1 in Xenopus oocytes and Chinese hamster ovary (CHO) cells. For most di- and tripeptides tested, the Kt was in the micromolar range, except Lys-Lys and Lys-Trp-Lys. Northern analysis demonstrated that cPepT1 is expressed strongly in the small intestine, and at lower levels in kidney and cecum. These results demonstrated the presence and functions of a peptide transporter in chickens. cPepT1 mRNA abundance was evaluated in response to developmental and dietary regulations. In Experiment 1, eggs at incubation day 18 (E18) and Cobb chicks after hatch (d 0) were sampled before treatments. Three groups of chicks were fed diets containing 12, 18, or 24% crude protein (CP). Feed intake of chicks fed the 18 or 24% CP diets was restricted to that of chicks fed the 12% CP diet. In Experiment 2, a fourth group with free access to the 24% CP diet was added. cPepT1 mRNA abundance was quantified from northern blots. By d 0, there was a 50-fold increase in cPepT1 mRNA abundance compared with E 18. In chicks fed the 12% CP diet, cPepT1 mRNA abundance decreased throughout the 35 d. Chicks fed 18 or 24% CP diets showed an increase in cPepT1 mRNA abundance with time. In chicks with free access to the 24% CP diet, cPepT1 mRNA decreased until d 14 but returned to an intermediate level at d 35. Our results indicate that cPepT1 mRNA is regulated by both dietary protein and developmental stage. To investigate the kinetics of an ovine peptide transporter (oPepT1), CHO cells were transfected with oPepT1 cDNA. Uptake of Gly-Sar by transfected cells was pH-dependent, concentration-dependent, and saturable. Competition studies showed that all di-, tri-, and tetra-peptides inhibited uptake of Gly-Sar. Pretreatment of the cells with staurosporine resulted in an increase in peptide transport. This increase was blocked by pretreatment with PMA. The results indicate that protein kinase plays a role in oPepT1 function. Advisors/Committee Members: Bloomquist, Jeffrey R. (committee member), Jiang, Honglin (committee member), Denbow, D. Michael (committee member), Wong, Eric A. (committeecochair), Webb, Kenneth E. Jr. (committeecochair).

Subjects/Keywords: Protein Kinase; Northern blot; Dietary protein; Development; PepT1; Peptide Transport

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APA (6^th Edition):

Chen, H. (2001). Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/29184

Chicago Manual of Style (16^th Edition):

Chen, Hong. “Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line.” 2001. Doctoral Dissertation, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/29184.

MLA Handbook (7^th Edition):

Chen, Hong. “Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line.” 2001. Web. 03 Mar 2021.

Vancouver:

Chen H. Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line. [Internet] [Doctoral dissertation]. Virginia Tech; 2001. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/29184.

Council of Science Editors:

Chen H. Cloning, Expression, and Developmental and Dietary Regulations of a Chicken Intestinal Peptide Transporter and Characterization and Regulation of an Ovine Gastrointestinal Peptide Transporter Expressed in a Mammalian Cell Line. [Doctoral Dissertation]. Virginia Tech; 2001. Available from: http://hdl.handle.net/10919/29184

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