Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice.

Satoh M, Hoshino M, Fujita K, Iizuka M, Fujii S, Clingan CS, Van Kaer L, Iwabuchi K
Sci Rep. 2016 6: 28473

PMID: 27329323 · PMCID: PMC4916414 · DOI:10.1038/srep28473

It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely defined. In this study, we have demonstrated that 3T3-L1 adipocytes can present endogenous ligands to NKT cells, leading to IFN-γ production, which in turn, stimulated 3T3-L1 adipocytes to enhance expression of CD1d and CCL2, and decrease expression of adiponectin. Furthermore, adipocyte-specific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensitivity in mice fed a high-fat diet (HFD). Accordingly, NKT cells were less activated, IFN-γ production was significantly reduced, and levels of adiponectin were increased in these animals as compared with control mice on HFD. Importantly, macrophage recruitment into the adipose tissue of adipocyte-specific CD1d-deficient mice was significantly blunted. These findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction of inflammation and functional modulation of adipose tissue that leads to obesity.

MeSH Terms (21)

3T3-L1 Cells Adipocytes Adiponectin Animals Antigen Presentation Antigens, CD1d B7-1 Antigen Diet, High-Fat Disease Models, Animal Disease Progression Galactosylceramides Insulin Resistance Interferon-gamma Lymphocyte Activation Macrophage Activation Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Natural Killer T-Cells Obesity

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