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University of New South Wales
1.
Tonks, Katherine.
Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus.
Degree: Clinical School - St Vincent's Hospital, 2014, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/55479 
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37808/SOURCE02?view=true
► Insulin resistance is central to type 2 diabetes, and its relationships to adiposity are complex. Some obese humans are protected from insulin resistance and the…
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▼ Insulin resistance is central to type 2 diabetes, and its relationships to adiposity are complex. Some obese humans are protected from insulin resistance and the Metabolic Syndrome. By studying these individuals we attempt to identify factors protective against insulin resistance, distinguishing between insulin resistance, hyperglycaemia, and adiposity per se.We recruited 81 individuals, in 4 groups: lean control (n=23, BMI ≤ 25 kg/m2, HOMA<2), Obresistant (n=21, BMI>25 kg/m2, HOMA>3), T2D (n=21), and Obsensitive (n=16, BMI>25 kg/m2, HOMA<1.5). Obresistant, T2D and Obsensitive were matched for waist:hip ratio, total body fat %, central fat %, fat content of legs (kg) and average subcutaneous fat cm2. Obsensitive were as insulin-sensitive as the lean by HOMA (1.2±0.3 vs 1.2±0.4, respectively) and hyperinsulinaemic-euglycaemic clamp (GIR 86±36 vs 92±23 μmol/min/kg FFM, respectively) despite twice their total and central fat. Obresistant and T2D had significantly lower GIR/FFM (61±24 vs 44±13 µmol/min/kgFFM, respectively). Chapter 3 demonstrates that adiponectin and FGF21 levels, as well as visceral and hepatic fat, are strong predictors of insulin resistance in human muscle. Chapter 4 shows that pAkt is lower in Obresistance and T2D, but pAS160 (downstream of pAkt) is lower in all overweight/obese groups, indicating that adiposity may influence insulin signalling-mediated insulin resistance. Adiponectin strongly mirrors pAkt, and FABP4 correlates with pAS160.Chapter 5 shows that urinary catecholamines correlate to fat mass rather than insulin sensitivity. Obesity may lead to higher sympathetic drive, with compensatory parasympathetic drive lost in Obresistant (maintained in Obsensitive). Once T2D develops sympathetic drive is also blunted. Chapter 6 demonstrates that plasma and muscle ceramides are associated with insulin resistance and visceral adiposity. There were negative associations between ceramides and insulin-stimulated pAkt309, and baseline adiponectin; and positive associations with FGF21, FABP4 and LCN2. A number of pathways may augment insulin sensitivity: THC 24:1, 24:0 and 22:0 negatively associate with deep subcutaneous and hepatic adiposity in women; GM3 22:0 and SM 33:1 through (superficial) subcutaneous fat; and SM 32:2 through lower deep subcutaneous fat and FABP4. No previous study has definitively demonstrated insulin-sensitivity at a molecular level in muscle of Obsensitive humans. Their study raises potential diagnostic or therapeutic avenues.
Advisors/Committee Members: Greenfield, Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, James, David, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.
Subjects/Keywords: Insulin sensitive obesity; Insulin reistance; Diabetes mellitus; Obesity
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APA (6th Edition):
Tonks, K. (2014). Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55479 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37808/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Tonks, Katherine. “Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus.” 2014. Doctoral Dissertation, University of New South Wales. Accessed January 16, 2021.
http://handle.unsw.edu.au/1959.4/55479 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37808/SOURCE02?view=true.
MLA Handbook (7th Edition):
Tonks, Katherine. “Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus.” 2014. Web. 16 Jan 2021.
Vancouver:
Tonks K. Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2021 Jan 16].
Available from: http://handle.unsw.edu.au/1959.4/55479 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37808/SOURCE02?view=true.
Council of Science Editors:
Tonks K. Defining the insulin signalling defects in insulin resistance and type 2 diabetes mellitus. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/55479 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37808/SOURCE02?view=true
University of New South Wales
2.
Chen, Daniel.
Insulin-sensitive Obesity.
Degree: Clinical School - St Vincent's Hospital, 2015, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/55745
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true
► Introduction: While insulin resistance and obesity coexist, some obese individuals remain insulin-sensitive. We examined phenotypic and metabolic factors associated with insulin sensitivity in both muscle…
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▼ Introduction: While insulin resistance and obesity coexist, some obese individuals remain insulin-sensitive. We examined phenotypic and metabolic factors associated with insulin sensitivity in both muscle and liver in obese individuals. Methods: Sixty-four non-diabetic obese adults (29 males) underwent hyperinsulinaemic (15 and 80 mU/m2/min)-euglycaemic clamps with deuterated glucose. Top tertile subjects for glucose infusion rate during the high-dose insulin clamp (GIRHI) were assigned Musclesen and those in the lower two tertiles were assigned Muscleres. Secondarily, top tertile subjects for endogenous glucose production (EGP) suppression during the low-dose insulin clamp were deemed Liversen and the remainder Liverres. Clinical and laboratory parameters, muscle sympathetic nervous activity (MSNA) and visceral, subcutaneous, liver and pancreatic fat were compared.Results: Musclesen and Muscleres had similar body mass index and total fat (P ≥ 0.12), but Musclesen had lower HbA1c (P < 0.001) and systolic (P = 0.01) and diastolic (P = 0.03) blood pressure (BP). Despite similar subcutaneous fat (P = 0.83), Musclesen had lower visceral (P < 0.001) and liver (P < 0.001) fat. Liversen had lower visceral (P < 0.01) and liver (P < 0.01) fat and CRP (P=0.02) than Liverres. When subjects were grouped by both GIRHI and EGP suppression, insulin sensitivity at either muscle or liver conferred apparent protection from the adverse metabolic features that characterized subjects insulin-resistant at both sites. HDL-cholesterol, 1-hour glucose, systolic BP and triglycerides explained 54% of the variance in muscle insulin sensitivity. In men (but not women), MSNA burst frequency correlated inversely with liver insulin sensitivity (r = -0.53, P = 0.02) and positively with the C-reactive protein (CRP) and fibroblast growth factor (FGF)-19 (r = 0.57, P = 0.006 and r = -0.47, P = 0.03, respectively). Conclusions: Obese subjects who were insulin-sensitive at muscle and/or liver exhibited favourable metabolic features, including lower BP, liver and visceral adiposity. Basal sympathetic nerve activity related to liver insulin sensitivity in men, but not in women. MSNA associated with the circulating hepatokines CRP and FGF-19, suggesting a potential hepato-endocrine-autonomic axis. This study identifies factors associated with, and possibly contributing to, insulin sensitivity in obesity.
Advisors/Committee Members: Greenfield, Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Chisholm, Don, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.
Subjects/Keywords: Obesity; Insulin sensitivity
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APA (6th Edition):
Chen, D. (2015). Insulin-sensitive Obesity. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true
Chicago Manual of Style (16th Edition):
Chen, Daniel. “Insulin-sensitive Obesity.” 2015. Doctoral Dissertation, University of New South Wales. Accessed January 16, 2021.
http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true.
MLA Handbook (7th Edition):
Chen, Daniel. “Insulin-sensitive Obesity.” 2015. Web. 16 Jan 2021.
Vancouver:
Chen D. Insulin-sensitive Obesity. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2021 Jan 16].
Available from: http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true.
Council of Science Editors:
Chen D. Insulin-sensitive Obesity. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55745 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38988/SOURCE01?view=true
University of New South Wales
3.
Tang, Alice.
Insulin-Sensitive Obesity: Prospective and Interventional Studies.
Degree: Clinical School - St Vincent's Hospital, 2017, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/58936
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true
► BACKGROUND: Individuals with metabolically healthy/insulin-sensitive obesity (MHO/Obsen) have been shown to have a comparable metabolic profile to lean individuals. However, longitudinal change in metabolic parameters…
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▼ BACKGROUND: Individuals with metabolically healthy/insulin-sensitive obesity (MHO/Obsen) have been shown to have a comparable metabolic profile to lean individuals. However, longitudinal change in metabolic parameters in those with MHO/Obsen has not been comprehensively delineated with the gold-standard measure of insulin-sensitivity, the hyperinsulinaemic-euglycaemic clamp. The response of MHO/ Obsen cohorts to weight loss is also unclear. This study investigates the metabolic changes in the Obsen phenotype over time and in response to weight loss. METHODS: A cohort of 124 individuals was carefully phenotyped 6 years ago and categorised into lean, overweight/obese insulin-sensitive (Obsen) or resistant (Obres, using gender based median insulin-sensitivity cut-offs) and type 2 diabetes mellitus (T2DM). Sixty-nine participants were followed up in this study. A subcohort (n = 13) also underwent a 16-week caloric restriction intervention. A comprehensive assessment of metabolic health, including insulin sensitivity (using hyperinsulinaemic-euglcyaemic clamp), body fat composition, serum/plasma metabolic markers, energy metabolism and lifestyle parameters, was performed.RESULTS: There was an increase in total body fat, visceral adipose tissue mass, blood pressure and adipose tissue insulin resistance and a decrease in resting metabolic rate in the whole cohort over 6 years. Insulin sensitivity appeared to decrease over time in Obsen compared to the other groups. Physical activity increased and sugar intake decreased in Obres and T2DM. Saturated fat and trans-fat intake increased in the Obsen group. Insulin sensitivity in the 6 years prior to weight loss was inversely correlated to the change in insulin sensitivity induced by weight loss. Insulin sensitivity immediately prior to weight loss was inversely correlated to the change in resting metabolic rate induced by weight loss.CONCLUSION: Obsen is not an enduring phenotype over 6 years. Hence, clinical intervention should target all individuals with overweight/obesity, irrespective of apparent metabolic health. However, further investigation into the role that insulin sensitivity plays in the response to weight loss is required to ensure optimum management in Obsen individuals.
Advisors/Committee Members: Greenfield, Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Samocha-Bonet, Dorit, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.
Subjects/Keywords: Insulin resistance; Obesity; Insulin sensitivity
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APA (6th Edition):
Tang, A. (2017). Insulin-Sensitive Obesity: Prospective and Interventional Studies. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Tang, Alice. “Insulin-Sensitive Obesity: Prospective and Interventional Studies.” 2017. Doctoral Dissertation, University of New South Wales. Accessed January 16, 2021.
http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true.
MLA Handbook (7th Edition):
Tang, Alice. “Insulin-Sensitive Obesity: Prospective and Interventional Studies.” 2017. Web. 16 Jan 2021.
Vancouver:
Tang A. Insulin-Sensitive Obesity: Prospective and Interventional Studies. [Internet] [Doctoral dissertation]. University of New South Wales; 2017. [cited 2021 Jan 16].
Available from: http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true.
Council of Science Editors:
Tang A. Insulin-Sensitive Obesity: Prospective and Interventional Studies. [Doctoral Dissertation]. University of New South Wales; 2017. Available from: http://handle.unsw.edu.au/1959.4/58936 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:47978/SOURCE02?view=true
University of New South Wales
4.
Kozan, Pinar.
The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.
Degree: St Vincent's Clinical School, 2018, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/59592
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true
► Background: High dietary acid load relates to increased risk of type 2 diabetes in epidemiological studies. We aimed to investigate whether buffering a high acid…
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▼ Background: High dietary acid load relates to increased risk of type 2 diabetes in epidemiological studies. We aimed to investigate whether buffering a high acid load meal with an alkalising treatment changes post meal glucose metabolism. Methods: Non-diabetic participants (n=32) were randomized to receive either NaHCO3 1680mg or placebo, followed by a high acid load meal in a double-blind placebo-controlled crossover (1-4 weeks apart) study. Thirty (20 males) participants completed the study. Venous blood pH, serum bicarbonate, blood glucose, serum insulin, C-peptide, non-esterified fatty acid (NEFA), and plasma glucagon-like peptide-1 (GLP-1) concentrations were measured at baseline (fasting) and at 15-30min intervals for 3h post meal. Results: The treatment was well tolerated. Venous blood pH declined in the first 15min post meal with the placebo (p=0.001), but not with NaHCO3 (p=0.86) and remained lower with the placebo for 3h (pinteraction=0.04). The iAUC of pH was significantly higher following the NaHCO3 treatment versus the placebo (p=0.02). However, postprandial glucose, insulin, C-peptide, NEFA and GLP-1 were not different between treatments (pinteraction≥0.07). Conclusions: An alkalising medication administered pre-meal has no acute effect on glycaemia and insulin response in healthy individuals. Long-term interventions in at-risk populations are necessary to investigate the effect of sustained alkalisation on glucose metabolism.
Advisors/Committee Members: Greenfield , Jerry, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Samocha-Bonet, Dorit, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.
Subjects/Keywords: acid-base homeostasis; alkaline diet; dietary acid load; type 2 diabetes; sodium bicarbonate; postprandial glycaemia
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APA ·
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APA (6th Edition):
Kozan, P. (2018). The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Kozan, Pinar. “The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.” 2018. Masters Thesis, University of New South Wales. Accessed January 16, 2021.
http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true.
MLA Handbook (7th Edition):
Kozan, Pinar. “The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans.” 2018. Web. 16 Jan 2021.
Vancouver:
Kozan P. The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. [Internet] [Masters thesis]. University of New South Wales; 2018. [cited 2021 Jan 16].
Available from: http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true.
Council of Science Editors:
Kozan P. The effect of buffering a high acid load meal with sodium bicarbonate on postprandial glucose metabolism in humans. [Masters Thesis]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/59592 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:49042/SOURCE02?view=true
. 
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