Obesity in the pathogenesis of type 2 diabetes

Caroline Day, Clifford J. Bailey

Research output: Contribution to journalArticle

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 TNF, 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.
Original languageEnglish
Pages (from-to)55-61
Number of pages7
JournalBritish Journal of Diabetes and Vascular Disease
Volume11
Issue number2
DOIs
Publication statusPublished - Mar 2011

Fingerprint

Type 2 Diabetes Mellitus
Insulin Resistance
Fatty Acids
Obesity
Adipokines
Abdominal Obesity
Ceramides
Adiponectin
Diglycerides
Adiposity
Islets of Langerhans
Hyperglycemia
Protein Kinase C
Adipose Tissue
Interleukin-6
Protein Isoforms
Fats
Insulin
Lipids
Glucose

Keywords

  • adipokines
  • type 2 diabetes
  • obesity
  • insulin resistance
  • adipose cytokines

Cite this

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Obesity in the pathogenesis of type 2 diabetes. / Day, Caroline; Bailey, Clifford J.

In: British Journal of Diabetes and Vascular Disease, Vol. 11, No. 2, 03.2011, p. 55-61.

Research output: Contribution to journalArticle

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