CD36 genetics and the metabolic complications of obesity

The review summarizes our current understanding of the function of the fatty acid translocase, CD36, in lipid metabolism with an emphasis on the influence of CD36 genetic variants and their potential contribution to obesity-related complications.

Studies in rodents implicate CD36 in a number of metabolic pathways with relevance to obesity and its associated complications. These include pathways related to fat utilization such as taste perception, intake, intestinal processing, and storage in adipose tissue. Dysfunction in these pathways, coupled with the ability of CD36 to transduce intracellular signals that initiate inflammation in response to excess fat supply, promotes metabolic pathology. In the last few years, the relevance of discoveries in rodents to humans has been highlighted by genetic studies, which identified common CD36 variants that influence circulating lipid levels and cardiometabolic phenotypes.

Recent genetic studies suggest that CD36 plays an important role in lipid metabolism in humans and may be involved in obesity-related complications. These findings may accelerate the translation of CD36 metabolic functions determined in rodents to humans. Importantly, these studies highlight the potential utility of assessing CD36 expression and common single-nucleotide polymorphism genotypes.