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Perilipin 3 Deficiency Stimulates Thermogenic Beige Adipocytes Through PPARα Activation.

Diabetes. 2018 May;67(5):791-804. Epub 2018 Feb 13
Yun Kyung Lee 1 , Jee Hyung Sohn 1 , Ji Seul Han 1 , Yoon Jeong Park 2 , Yong Geun Jeon 1 , Yul Ji 1 , Knut Tomas Dalen 3 , Carole Sztalryd 4 , Alan R Kimmel 5 , Jae Bum Kim 2
Yun Kyung Lee 1 , Jee Hyung Sohn 1 , Ji Seul Han 1 , Yoon Jeong Park 2 , Yong Geun Jeon 1 , Yul Ji 1 , Knut Tomas Dalen 3 , Carole Sztalryd 4 , Alan R Kimmel 5 , Jae Bum Kim 2
+ et al

[No authors listed]

Author information
  • 1 Department of Biological Sciences, National Creative Research Initiatives Center for Adipose Tissue Remodeling, Institute of Molecular Biology and Genetics, Seoul National University, Seoul, South Korea.
  • 2 Department of Biophysics and Chemical Biology, Seoul National University, Seoul, South Korea.
  • 3 Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
  • 4 Department of Medicine, University of Maryland School of Medicine, Baltimore, MD.
  • 5 Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.

摘要


Beige adipocytes can dissipate energy as heat. Elaborate communication between metabolism and gene expression is important in the regulation of beige adipocytes. Although lipid droplet (LD) binding proteins play important roles in adipose tissue biology, it remains unknown whether perilipin 3 (Plin3) is involved in the regulation of beige adipocyte formation and thermogenic activities. In this study, we demonstrate that Plin3 ablation stimulates beige adipocytes and thermogenic gene expression in inguinal white adipose tissue (iWAT). Compared with wild-type mice, Plin3 knockout mice were cold tolerant and displayed enhanced basal and stimulated lipolysis in iWAT, inducing peroxisome proliferator-activated receptor α (PPARα) activation. In adipocytes, Plin3 deficiency promoted PPARα target gene and uncoupling protein 1 expression and multilocular LD formation upon cold stimulus. Moreover, fibroblast growth factor 21 expression and secretion were upregulated, which was attributable to activated PPARα in Plin3-deficient adipocytes. These data suggest that Plin3 acts as an intrinsic protective factor preventing futile beige adipocyte formation by limiting lipid metabolism and thermogenic gene expression.