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[From obesity to diabetes].

R Stöckli1, U Keller

  • 1Abteilung für Endokrinologie, Diabetologie und Klinische Ernährung, Departement Innere Medizin, Universitätskliniken Kantonsspital, Basel.

Therapeutische Umschau. Revue Therapeutique
|September 19, 2002
PubMed
Summary

Obesity drives insulin resistance and type 2 diabetes. Lifestyle changes like weight loss and exercise are crucial for prevention, while medications like thiazolidinediones improve glucose control.

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Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Adipose Tissue Biology

Context:

  • Obesity is a primary risk factor for insulin resistance and type 2 diabetes.
  • Adipocytes function as an endocrine system, secreting hormones that influence insulin sensitivity.
  • Visceral adipose tissue impacts cortisol metabolism, potentially exacerbating insulin resistance.

Purpose:

  • To review the role of adipocytes in insulin resistance.
  • To discuss the mechanisms by which obesity contributes to type 2 diabetes.
  • To highlight therapeutic strategies targeting adipocyte function and metabolism.

Summary:

  • Adipocytes release adiponectin, resistin, TNF-alpha, and IL-6, contributing to insulin resistance.
  • Free fatty acids impair glucose metabolism and cause lipotoxicity.
  • Thiazolidinediones (glitazones) activate PPAR-gamma, reducing resistin and increasing adiponectin, improving glucose homeostasis.

Impact:

  • Understanding adipocyte endocrine function offers new therapeutic targets for diabetes.
  • Lifestyle interventions (weight loss, exercise) are effective in preventing type 2 diabetes.
  • Pharmacological agents like glitazones demonstrate potential in managing glucose metabolism.

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