Macrophage infiltration and cytokine release in adipose tissue: Angiogenesis or inflammation?

Diabetology International 11/2010; 1(1):26-34. DOI: 10.1007/s13340-010-0003-x


The observation that obese adipose tissue was infiltrated by macrophages triggered the concept that type 2 diabetes is a low-grade
inflammatory disease. In this review, we re-evaluate the role of macrophage infiltration, TNFα secretion and IKKβ/JNK signalling
in insulin resistance, and put forward the hypothesis that these intermediates are important mediators of adipose tissue angiogenesis.
Expansion of adipose tissue vasculature is essential to support adipose tissue growth during development and adipose tissue
expansion in adulthood. We propose that a major role of so-called pro-inflammatory adipokines is to stimulate adipose tissue
angiogenesis to support the nutrient requirements of expanding fat depots. Inhibition of angiogenesis overrides insulin resistance
and obesity not by blocking the peripheral effects of the inflammatory pathway on insulin resistance, but rather by central
effects on food intake. This unveils a possible feedback loop involving adipose angiogenesis and central regulation of food
intake that is independent of a classical immune response.

KeywordsAngiogenesis-Macrophages-Inflammation-Adipose tissue-Insulin resistance-Adipokines

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