Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5618690 | Molecular Metabolism | 2016 | 13 Pages |
Abstract
We conclude that Hig2 localizes to LDs in adipocytes, promoting adipose tissue lipid deposition and that its selective deficiency in active brown/beige adipose tissue mediates improved glucose tolerance at 23 °C. Reversal of this phenotype at thermoneutrality in the absence of detectable changes in energy expenditure, adipose mass, or liver triglyceride suggests that Hig2 deficiency triggers a deleterious endocrine or neuroendocrine pathway emanating from brown/beige fat cells.
Keywords
Simpson-Golabi-Behmel syndromeFFASGBSIWATGTTSVFHFDBATRERNEFAeWATUcp1Adipocyteinsulin tolerance testFree fatty acidNon-esterified fatty acidITTepididymal white adipose tissueinguinal white adipose tissueWAT, White adipose tissuebrown adipose tissuetriglycerideglucose tolerance testHigh fat dietlipid dropletLipolysisObesityRespiratory exchange ratiouncoupling protein 1WATStromal vascular fraction
Related Topics
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Neuroscience
Endocrine and Autonomic Systems
Authors
Marina T. DiStefano, Rachel J. Roth Flach, Ozlem Senol-Cosar, Laura V. Danai, Joseph V. Virbasius, Sarah M. Nicoloro, Juerg Straubhaar, Sezin Dagdeviren, Martin Wabitsch, Olga T. Gupta, Jason K. Kim, Michael P. Czech,