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Insulin resistance in obesity: Targe...

Fealy, Ciaran E.

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Insulin resistance in obesity: Targeting the molecular mechanisms of metabolic disease.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Insulin resistance in obesity: Targeting the molecular mechanisms of metabolic disease./
Author:	Fealy, Ciaran E.
Description:	208 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.
Contained By:	Dissertation Abstracts International77-10B(E).
Subject:	Cellular biology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10109150
ISBN:	9781339724515

Insulin resistance in obesity: Targeting the molecular mechanisms of metabolic disease.
Fealy, Ciaran E.

Insulin resistance in obesity: Targeting the molecular mechanisms of metabolic disease. - 208 p.

Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.

Thesis (Ph.D.)--Kent State University, 2016.

The prevalence of obesity has been increasing rapidly over the past 30 years such that obesity-associated metabolic diseases including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D) are now among the leading causes of morbidity and mortality. This makes the discovery of novel, practical therapies for prevention and treatment, along with better understanding of the mechanisms that link obesity to metabolic disease, the most significant challenge for biomedical research in the 21st century. Insulin resistance is a common pathology underlying the development of obesity associated metabolic disease and is a target for disease progression. Exercise has long been recognized as an effective tool for managing glycemic control and its use in research provides insight into the mechanisms that contribute to insulin resistance. We used an exercise approach to investigate the effect of exercise training, independent of weight loss, on markers of hepatocyte apoptosis in individuals with NAFLD. Our data indicate that hepatocyte apoptosis is reduced following 7 days of exercise training. We also examined the efficacy of a novel high intensity exercise program for improving insulin sensitivity and reducing cardiometabolic risk in T2D. We concluded that CrossFit exercise reduces insulin resistance and cardiovascular risk in T2D. We also used an exercise approach to investigate a novel target that may link mitochondrial dysfunction to insulin resistance. We demonstrated that the activation of the mitochondrial fission mediator dynamin-related protein-1 was reduced by exercise in insulin resistant muscle and subsequent cell culture experiments provide evidence that this may be linked to improvements in insulin signalling and mitochondrial coupling efficiency.

ISBN: 9781339724515Subjects--Topical Terms:

3172791
Cellular biology.

Insulin resistance in obesity: Targeting the molecular mechanisms of metabolic disease.
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502 $a Thesis (Ph.D.)--Kent State University, 2016.
520 $a The prevalence of obesity has been increasing rapidly over the past 30 years such that obesity-associated metabolic diseases including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D) are now among the leading causes of morbidity and mortality. This makes the discovery of novel, practical therapies for prevention and treatment, along with better understanding of the mechanisms that link obesity to metabolic disease, the most significant challenge for biomedical research in the 21st century. Insulin resistance is a common pathology underlying the development of obesity associated metabolic disease and is a target for disease progression. Exercise has long been recognized as an effective tool for managing glycemic control and its use in research provides insight into the mechanisms that contribute to insulin resistance. We used an exercise approach to investigate the effect of exercise training, independent of weight loss, on markers of hepatocyte apoptosis in individuals with NAFLD. Our data indicate that hepatocyte apoptosis is reduced following 7 days of exercise training. We also examined the efficacy of a novel high intensity exercise program for improving insulin sensitivity and reducing cardiometabolic risk in T2D. We concluded that CrossFit exercise reduces insulin resistance and cardiovascular risk in T2D. We also used an exercise approach to investigate a novel target that may link mitochondrial dysfunction to insulin resistance. We demonstrated that the activation of the mitochondrial fission mediator dynamin-related protein-1 was reduced by exercise in insulin resistant muscle and subsequent cell culture experiments provide evidence that this may be linked to improvements in insulin signalling and mitochondrial coupling efficiency.
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