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Coordinated Regulation of Adipose Tissue Macrophages by Cellular and Nutritional Signals
  1. Daniel Har, BS,
  2. Michelle Carey, MD, MPH,
  3. Meredith Hawkins, MD, MS
  1. From the Division of Endocrinology, Department of Medicine and Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY.
  1. Received March 25, 2013.
  2. Accepted for publication May 6, 2013.
  3. Reprints: Meredith Hawkins, MD, MS, Albert Einstein College of Medicine, 1300 Morris Park Ave, Belfer 709, Bronx, NY 10461. E-mail: meredith.hawkins{at}einstein.yu.edu.
  4. This symposium was supported in part by a grant from the National Center for Research Resources (R13 RR023236).

Abstract

The current epidemic of obesity is fueling a global rise in non-communicable diseases, including type 2 diabetes mellitus, atherothrombotic disease, and cancer. Obesity is associated with systemic inflammation, with various fat-derived inflammatory factors being implicated in the pathophysiology of insulin resistance. The infiltration of various types of inflammatory cells into adipose tissue seems to be an important mechanism whereby nutrient excess contributes to systemic insulin resistance. In particular, adipose tissue macrophages are abundant in obese adipose tissue, and may be the source of the majority of fat-derived circulating inflammatory factors. This review examines recent studies exploring mechanisms whereby cellular and nutritional signals mediate macrophage recruitment to adipose tissue and their pro-inflammatory activation.

Key Words
  • regulation of adipose tissue macrophages
  • cytokines
  • free fatty acids

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