Nck2, an unexpected regulator of adipogenesis.
The regulation of adipose tissue expansion by adipocyte hypertrophy and/or hyperplasia is the topic of extensive investigations given the potential differential contribution of the 2 processes to the development of numerous chronic diseases associated with obesity. We recently discovered that the loss-of-function of the Src homology domain-containing protein Nck2 in mice promotes adiposity accompanied with adipocyte hypertrophy and impaired function, and enhanced adipocyte differentiation in vitro. Moreover, in severely-obese human's adipose tissue, we found that Nck2 expression is markedly downregulated. In this commentary, our goal is to expand upon additional findings providing further evidence for a unique Nck2-dependent mechanism regulating adipogenesis. We propose that Nck2 should be further investigated as a regulator of the reliance of white adipose tissue on hyperplasia versus hypertrophy during adipose tissue expansion, and hence, as a potential novel molecular target in obesity.
['Haider|N|N|', 'Dusseault|J|J|', 'Rudich|A|A|', 'Larose|L|L|']
D041721:3T3-L1 Cells D048868:Adaptor Proteins, Signal Transducing D017667:Adipocytes D050156:Adipogenesis D000273:Adipose Tissue D052436:Adipose Tissue, White D050154:Adiposity D000818:Animals D015536:Down-Regulation D006984:Hypertrophy D051379:Mice D009765:Obesity D015513:Oncogene Proteins
Adipogenesis adipocyte differentiation 3T3-L1 and SGBS preadipocytes PERK activation and signaling PPARγ regulation Src homology adaptor protein Nck2