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 Presentation

"Obesity and Insulin Resistance: Precursors for Type 2 Diabetes"

Prof. John Prins (biography)
English - 2005-09-11 - 35 minutes
(33 slides)
(3 questions)

Summary :
Obesity is commonly associated with a number of clinical features and /or pathologies that, collectively, have been termed the “metabolic syndrome”. Early definitions of the metabolic syndrome as proposed by Reaven and the World Health Organization regarded insulin resistance as the central and cardinal feature. More recent definitions from the National Cholesterol Education Program and the International Diabetes Federation have regarded central obesity (as assessed by waist circumference) as the prominent abnormality. Overall however, the strong relationship between obesity and insulin resistance in most patients underpins the metabolic syndrome and the associated risk of type 2 diabetes and vascular disease.

Except in situations of weight loss, the metabolic syndrome is a progressive disorder, with a major outcome being type 2 diabetes. Interventions that slow the rate of progression commonly reduce insulin resistance, supporting the importance of this parameter in disease progression.

Work over the last decade has lead to the recognition that adipokines are major mediators of the relationship between obesity and metabolic dysfunction. These secreted products from adipose tissue have direct and indirect effects to regulate appetite, glucose, lipid and protein metabolism, and cellular inflammation. It is now recognized that adipokine production is not regulated in obesity, but it has also been shown that it can be normalized with weight loss. The vast majority of adipokines are secreted in excess in obese states, leading to progressively greater metabolic dysfunction. With respect to glucose metabolism and insulin resistance, adipose production of TNF-alpha, leptin and steroid hormones all contribute to progressive insulin resistance. In addition, increased circulating free fatty acid levels and intracellular “ectopic” lipid storage further exacerbate metabolic dysfunction, inflammation, pancreatic beta cell compromise, and insulin resistance. An important exception to this situation is adiponectin, an adipokine with insulin sensitizing and anti-inflammatory properties. Obesity and the metabolic syndrome are adiponectin-deficient states, and animal data suggests the exciting possibility that strategies to increase circulating adiponectin levels may provide substantial benefit.

Untreated metabolic syndrome is a progressive disorder in most patients, leading to the acquisition of increasing numbers of related pathologies of increasing severity. Common outcomes include type 2 diabetes, due to the dual abnormalities of insulin resistance and beta cell dysfunction, vascular disease and malignancy. Given the scale of this clinical problem in most societies, a top medical research priority must be to develop and evaluate strategies to halt or slow the progressive nature of the metabolic syndrome and its related disorders.

Learning objectives :
After viewing this presentation the participant will be able to discuss:

- How excess energy causes events contributing to type 2 diabetes
- The role of adipokines in obesity and metabolic syndrome: adiponectin

   


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