Laminin a4 Deficient Mice Exhibit Decreased Capacity for Adipose Tissue Expansion and Weight Gain

Vaicik M.K., Thyboll Kortesmaa J., Movérare-Skrtic S., Kortesmaa J., Soininen R., Bergström G., Ohlsson C., Chong L.Y., Rozell B., Emont M., Cohen R.N., Brey E.M., Tryggvason K.PLOS ONE, 2014

Staining was performed for known adipose tissue BM proteins. In wild-type control mice the a2 and a4 chains of laminin were present in the BM surrounding mature adipocytes. Laminin a5 was not observed in mouse adipocyte BM. In this manuscript, we describe the role of laminin a4, a specialized ECM protein surrounding adipocytes, on weight gain and adipose tissue function. Adipose tissue accumulation, lipogenesis, and structure were examined in mice with a null mutation of the laminin a4 gene (Lama42/2) and compared to wild-type (Lama4+/+) control animals. Lama42/2 mice exhibited reduced weight gain in response to both age and high-fat diet. Interestingly, the mice had decreased adipose tissue mass and altered lipogenesis in a depot-specific manner. In particular, epididymal adipose tissue mass was specifically decreased in knock-out mice, and there was also a defect in lipogenesis in this depot as well. In contrast, no such differences were observed in subcutaneous adipose tissue at 14 weeks. The results suggest that laminin a4 influences adipose tissue structure and function in a depot-specific manner.

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