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You searched for +publisher:"University of New South Wales" +contributor:("Chisholm, Don, Garvan Institute of Medical Research, Faculty of Medicine, UNSW"). Showing records 1 – 2 of 2 total matches.

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University of New South Wales

1. Chen, Daniel. Insulin-sensitive Obesity.

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

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

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 September 18, 2019. 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. 18 Sep 2019.

Vancouver:

Chen D. Insulin-sensitive Obesity. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2019 Sep 18]. 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

2. Ho, Kenneth Wai Kheong. Iron chelation for treating obesity and components of the metabolic syndrome.

Degree: Clinical School - St Vincent's Hospital, 2011, University of New South Wales

Epidemiological studies suggest a link between iron stores and components of the metabolic syndrome. Human subjects with ironoverload syndromes are more prone to obesity, diabetes and metabolic syndrome. Excess iron can generate Reactive Oxygen Species(ROS) resulting in insulin resistance and cell apoptosis. Iron chelation reduces diabetes in iron overload syndromes but effects onobesity and related metabolic variables are unknown in non-overloaded individuals. Hypoxia Inducible Factor- 1-alpha (HIF-1α) is atranscription factor up-regulated by hypoxia, which is also increased by iron chelation in-vitro. HIF-1α impacts lipid and whole bodymetabolism and cellular survival by improving glucose uptake, facilitating anaerobic glycolysis, and attenuating ROS.Hypothesis: That iron chelation may treat or prevent components of the metabolic syndrome via HIF-1 induction. This thesisinvestigated effects of iron chelators on murine models of obesity and diabetes: C57Bl/6 mice on high fat diet (HFD), ob/ob mice onchow diet, C57Bl/6 mice on chow, and Non-Obese Diabetic (NOD) mice. Two iron chelators were studied: Deferoxamine (DFO) as anintra-peritoneal injection weekly and continuous oral Deferasirox (DFS) mixed with diet. DFS-treatment had important metabolicbenefits, including reduction of weight gain in both male and female mice, from as early as 1 week, lasting throughout the period ofstudy (up to 9 months). Other benefits included lower plasma lipids, reduction of hepatic steatosis and improvement in insulinresistance. There was also improved beta cell function, evidenced by relatively preserved first phase insulin secretion and improvedglucose tolerance, particularly after prolonged high fat exposure. DFS treatment reduced hepatic iron and increased HIF-1α, associatedwith down-regulation of hepatic lipogene expression and improved insulin signalling gene expression. Importantly, DFS did not impairappetite and had no apparent toxicity. Treated mice gained weight as per normal chow-fed C57Bl/6 mice and were not renderedanaemic. Rather than reducing appetite, DFS appeared to increase appetite. This, together with increased core body temperature,suggested improved whole body metabolism. Metabolic chamber studies confirmed this, showing higher O2 consumption and CO2production in DFS-treated mice. These findings suggest iron chelation may be effective in improving the metabolic derangementsassociated with obesity. Advisors/Committee Members: Gunton, Jenny, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Laybutt, Ross, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Chisholm, Don, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: HIF-1a; Iron Chelation; Obesity

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

APA (6th Edition):

Ho, K. W. K. (2011). Iron chelation for treating obesity and components of the metabolic syndrome. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51290 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9971/SOURCE02?view=true

Chicago Manual of Style (16th Edition):

Ho, Kenneth Wai Kheong. “Iron chelation for treating obesity and components of the metabolic syndrome.” 2011. Doctoral Dissertation, University of New South Wales. Accessed September 18, 2019. http://handle.unsw.edu.au/1959.4/51290 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9971/SOURCE02?view=true.

MLA Handbook (7th Edition):

Ho, Kenneth Wai Kheong. “Iron chelation for treating obesity and components of the metabolic syndrome.” 2011. Web. 18 Sep 2019.

Vancouver:

Ho KWK. Iron chelation for treating obesity and components of the metabolic syndrome. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2019 Sep 18]. Available from: http://handle.unsw.edu.au/1959.4/51290 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9971/SOURCE02?view=true.

Council of Science Editors:

Ho KWK. Iron chelation for treating obesity and components of the metabolic syndrome. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51290 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9971/SOURCE02?view=true

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