Obesity in the pathogenesis of type 2 diabetes

Author:

Day Caroline1,Bailey Clifford J2

Affiliation:

1. Life and Health Sciences, Aston University, Birmingham, UK

2. Life and Health Sciences, Aston University, Birmingham, UK,

Abstract

Obesity, and especially visceral adiposity, escalates the development of insulin resistance and type 2 diabetes. Excess adipose tissue contributes to a chronic increase in circulating fatty acids reducing the usage of glucose as a source of cellular energy. Excess fatty acids also result in increased deposition of fat in muscle and liver, and increased metabolites such as diacylglycerol and ceramide which activate isoforms of protein kinase C that impede cellular insulin signalling. Chronically raised lipid levels also impair islet beta cell function, acting in conjuction with insulin resistance to aggravate hyperglycaemia. The detrimental effects of several adipokines such as TNFα, IL6 and RBP4, which are produced in excess by an increased adipose mass, and reduced production of adiponectin are further mechanisms through which obesity potentiates the development of type 2 diabetes.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Endocrinology, Diabetes and Metabolism,Internal Medicine

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