CD36: the common soil for inflammation in obesity and atherosclerosis?

Z Yang, XF Ming - Cardiovascular research, 2011 - academic.oup.com
Z Yang, XF Ming
Cardiovascular research, 2011academic.oup.com
Insulin resistance, a decreased metabolic responsiveness of peripheral organs and tissues
to insulin, is considered the central mechanism of metabolic syndrome, a cluster of
cardiovascular risk factors, including abdominal obesity, hypertension, a pro-atherogenic
lipid profile, a pro-thrombotic, pro-inflammatory state, and dysglycemia. Studies in recent
years have revealed the causal role of chronic low-grade inflammation in development of
obesity-associated insulin resistance in animal models. 1 Since chronic inflammation also …
Insulin resistance, a decreased metabolic responsiveness of peripheral organs and tissues to insulin, is considered the central mechanism of metabolic syndrome, a cluster of cardiovascular risk factors, including abdominal obesity, hypertension, a pro-atherogenic lipid profile, a pro-thrombotic, pro-inflammatory state, and dysglycemia. Studies in recent years have revealed the causal role of chronic low-grade inflammation in development of obesity-associated insulin resistance in animal models. 1 Since chronic inflammation also plays a pivotal role in atherosclerotic cardiovascular disease, 2 it is therefore considered to be the fundamental mechanistic link between insulin resistance and increased cardiovascular prevalence in obesity. Compelling evidence from numerous studies in animal models demonstrates that monocytes are recruited to adipose tissue during obesity and become macrophages through interaction with dysfunctional adipocytes. 3 Moreover, resident adipose tissue macrophages may switch their phenotype from the anti-inflammatory ‘alternative’(M2) to pro-inflammatory ‘classical’(M1) macrophages during expansion of adipose tissue in obesity. 4 Accumulation of macrophages and phenotypic switch from M2 to M1 macrophages has been suggested to play a determinant role in insulin resistance in obesity at least in mouse models. 3 Increased adipose tissue inflammation and macrophage infiltration have been confirmed in human obesity. 5 However, subset macrophage accumulation in human adipose tissue in obesity requires further characterization.
There is much interest in the question of what are the microenvironmental changes in adipose tissue in obesity that initiate and regulate adipose tissue inflammation. Adipocytes are highly active in secretion of numerous bioactive hormones called adipokines that exert profound endocrine and/or paracrine effects on different types of cells including macrophages and vascular wall cells, ie endothelial cells or smooth muscle cells. 6 It is proposed that adipocyte dysfunction reflected by imbalanced secretion of pro-inflammatory and anti-inflammatory adipokines contributes to insulin resistance,
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