Abstract
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.
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