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Role of the Immune System in Obesity-Associated Inflammation and Insulin Resistance

Authors
  • Nagai, Yoshinori
  • Takatsu, Kiyoshi
Type
Book
Journal
Nutrition in the Prevention and Treatment of Abdominal Obesity
Publication Date
Jan 01, 2014
Pages
281–293
Identifiers
DOI: 10.1016/B978-0-12-407869-7.00026-X
ISBN: 978-0-12-407869-7
Source
Elsevier
Keywords
License
Unknown

Abstract

Obesity-associated chronic tissue inflammation is a key contributory factor to type 2 diabetes mellitus, and a number of studies have clearly demonstrated that the immune system and metabolism are highly integrated. Recent advances in deciphering the various immune cells and signaling networks that link the immune and metabolic systems have contributed to our understanding of the pathogenesis of obesity-associated inflammation and may also inform new therapeutic strategies based on immunomodulation. Saturated free fatty acids derived from adipocytes are bioactive mediators that cause macrophages to induce proinflammatory cytokines that act on insulin target cells and insulin-producing pancreatic beta cells to impair insulin sensitivity and insulin secretion. Here, we discuss how various networks within the immune system underlie the etiology of obesity-associated inflammatory components of insulin resistance, with a particular focus on the central roles of macrophages in adipose tissue.

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