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

Extract

This editorial refers to ‘A CD36-dependent pathway enhances macrophage and adipose tissue inflammation and impairs insulin signalling’ by D.J. Kennedy et al., pp. 604–613, this issue.

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.