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Berardinelli-Seip congenital lipodystrophy 2 regulates adipocyte lipolysis,
browning, and energy balance in adult animals.
Authors Zhou H, Lei X, Benson T, Mintz J, Xu X, Harris RB, Weintraub NL, Wang X, Chen W
Submitted By Submitted Externally on 10/26/2016
Status Published
Journal Journal of lipid research
Year 2015
Date Published
Volume : Pages 56 : 1912 - 25
PubMed Reference 26269358
Abstract Mutations in BSCL2/SEIPIN cause Berardinelli-Seip congenital lipodystrophy type
2 (BSCL2), but the mechanisms whereby Bscl2 regulates adipose tissue function
are unclear. Here, we generated adipose tissue (mature) Bscl2 knockout (Ad-mKO)
mice, in which Bscl2 was specifically ablated in adipocytes of adult animals, to
investigate the impact of acquired Bscl2 deletion on adipose tissue function and
energy balance. Ad-mKO mice displayed reduced adiposity and were protected
against high fat diet-induced obesity, but not insulin resistance or hepatic
steatosis. Gene expression profiling and biochemical assays revealed increased
lipolysis and fatty acid oxidation in white adipose tissue (WAT) and brown
adipose tissue , as well as browning of WAT, owing to induction of cAMP/protein
kinase A signaling upon Bscl2 deletion. Interestingly, Bscl2 deletion reduced
food intake and downregulated adipose ß3-adrenergic receptor (ADRB3) expression.
Impaired ADRB3 signaling partially offsets upregulated browning-induced energy
expenditure and thermogenesis in Ad-mKO mice housed at ambient temperature.
However, this counter-regulatory response was abrogated under thermoneutral
conditions, resulting in even greater body mass loss in Ad-mKO mice. These
findings suggest that Bscl2 regulates adipocyte lipolysis and ß-adrenergic
signaling to produce complex effects on adipose tissues and whole-body energy


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