Nck2, an unexpected regulator of adipogenesis

N. Haider, J. Dusseault, A. Rudich, L. Larose

Research output: Contribution to journalComment/debate

3 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)154-160
Number of pages7
JournalAdipocyte
Volume6
Issue number2
DOIs
StatePublished - 3 Apr 2017

Keywords

  • 3T3-L1 and SGBS preadipocytes
  • Adipogenesis
  • PERK activation and signaling
  • PPARγ regulation
  • Src homology adaptor protein Nck2
  • adipocyte differentiation

ASJC Scopus subject areas

  • Histology
  • Cell Biology

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