Journal
CELL METABOLISM
Volume 11, Issue 6, Pages 479-492Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2010.04.013
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Funding
- Global COE Research Program
- Takeda Science Foundation
- Mitsukoshi Health and Welfare Foundation
- Sankyo Foundation of Life Science
- Mitsubishi Pharma Research Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Uehara Memorial Foundation
- Suzuken Memorial Foundation
- Kanae Foundation for the Promotion of Medical Science
- Astellas Foundation for Research on Metabolic Disorders
- Ono Medical Research Foundation
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Macrophages infiltrate adipose tissue in obesity and are involved in the induction of inflammation, thereby contributing to the development of obesity-associated metabolic disorders. Here, we show that the macrophage-derived soluble protein AIM is endocytosed into adipocytes via CD36. Within adipocytes, AIM associates with cytosolic fatty acid synthase (FAS), thereby decreasing FAS activity. This decreases lipid droplet size, stimulating the efflux of free fatty acids and glycerol from adipocytes. As an additional consequence of FAS inhibition, AIM prevents preadipocyte maturation. In vivo, the increase in adipocyte size and fat weight induced by high-fat diet (HFD) was accelerated in AIM-deficient (AIM(-/-)) mice compared to AIM(+/+) mice. Moreover, injection of recombinant AIM in AIM(-/-) mice suppresses the increase in fat mass induced by HFD. Interestingly, metabolic rates are comparable in AIM(-/-) and AIM(+/+) mice, suggesting that AIM specifically influences adipocyte status. Thus, this AIM function in adipocytes may be physiologically relevant to obesity progression.
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