TY - JOUR
T1 - Nck2, an unexpected regulator of adipogenesis
AU - Haider, N.
AU - Dusseault, J.
AU - Rudich, A.
AU - Larose, L.
N1 - Funding Information:
This work was funded by the Canadian Institutes for Health Research (CIHR, MOP-115045) grant to L.L. and by a grant from the Zavalkoff Foundation to A.R. and L.L. N.H. was supported by a student fellowship from the McGill University Health Center Research Institute (MUHC-RI).
Publisher Copyright:
© 2017 Taylor & Francis.
PY - 2017/4/3
Y1 - 2017/4/3
N2 - 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.
AB - 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.
KW - 3T3-L1 and SGBS preadipocytes
KW - Adipogenesis
KW - PERK activation and signaling
KW - PPARγ regulation
KW - Src homology adaptor protein Nck2
KW - adipocyte differentiation
UR - http://www.scopus.com/inward/record.url?scp=85060564608&partnerID=8YFLogxK
U2 - 10.1080/21623945.2017.1291102
DO - 10.1080/21623945.2017.1291102
M3 - Comment/debate
C2 - 28425845
AN - SCOPUS:85060564608
SN - 2162-3945
VL - 6
SP - 154
EP - 160
JO - Adipocyte
JF - Adipocyte
IS - 2
ER -