Insulin Resistance: Causes and Consequences

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

12 Scopus citations

Abstract

This review addresses aspects of the set of abnormalities of insulin action commonly referred to as "insulin resistance." The condition is created by a state of differential insulin resistance, with the metabolic effects of insulin being diminished, while the mitogenic effects of insulin on cellular growth and differentiation are relatively overexpressed. Adiposity is a major aspect of insulin resistance, with adipocyte secretory products playing an important role in decreasing insulin response. These include interleukin (IL) 6, tumor necrosis factor (TNF)-α, resistin, and interferon (IF)-γ. Adiponectin is an adipokine that acts to increase insulin sensitivity, with levels decreased in persons with insulin resistance. An additional potential mechanism is the association of obesity with the accumulation of macrophages in adipose tissue. The importance of the adipocyte is underscored by the effect of thiazolidinediones (TZD), an important group of oral hypoglycemic agents whose principal effect appears to be in increasing adipocyte differentiation and in increasing adipocyte insulin action. Interestingly, expression of macrophage-originated genes is downregulated after treatment with the TZD. The "insulin resistance syndrome" includes insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and increased risk of both diabetes and coronary heart disease. Associated illnesses include polycystic ovarian syndrome (PCOS), nonalcoholic fatty liver disease (NAFLD), malignancies including breast cancer, and sleep apnea. A number of groups have described sets of criteria for the syndrome, which can be used in clinical risk assessment.

Original languageEnglish
Title of host publicationInternational Review of Neurobiology
EditorsRonald Bradley, Adron Harris, Peter Jenner
Pages1-24
Number of pages24
DOIs
StatePublished - 2005

Publication series

NameInternational Review of Neurobiology
Volume65
ISSN (Print)0074-7742

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