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    Berardinelli-Seip Congenital Lipodystrophy 2/Seipin Is Not Required for Brown Adipogenesis but Regulates Brown Adipose Tissue Development and Function

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    Mol_Cell_Biol_2016_Zhou_2027_38.pdf
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    Description:
    FInal Published Version
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    Author
    Zhou, Hongyi
    Black, Stephen M.
    Benson, Tyler W.
    Weintraub, Neal L.
    Chen, Weiqin cc
    Affiliation
    Univ Arizona, Dept Med, Div Translat & Regenerat Med
    Issue Date
    2016-08-01
    
    Metadata
    Show full item record
    Publisher
    AMER SOC MICROBIOLOGY
    Citation
    Berardinelli-Seip Congenital Lipodystrophy 2/Seipin Is Not Required for Brown Adipogenesis but Regulates Brown Adipose Tissue Development and Function 2016, 36 (15):2027 Molecular and Cellular Biology
    Journal
    Molecular and Cellular Biology
    Rights
    Copyright © 2016, American Society for Microbiology. All Rights Reserved.
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    Brown adipose tissue (BAT) plays a unique role in regulating whole-body energy homeostasis by dissipating energy through thermogenic uncoupling. Berardinelli-Seip congenital lipodystrophy (BSCL) type 2 (BSCL2; also known as seipin) is a lipodystrophy-associated endoplasmic reticulum membrane protein essential for white adipocyte differentiation. Whether BSCL2 directly participates in brown adipocyte differentiation, development, and function, however, is unknown. We show that BSCL2 expression is increased during brown adipocyte differentiation. Its deletion does not impair the classic brown adipogenic program but rather induces premature activation of differentiating brown adipocytes through cyclic AMP (cAMP)/protein kinase A (PKA)-mediated lipolysis and fatty acid and glucose oxidation, as well as uncoupling. cAMP/PKA signaling is physiologically activated during neonatal BAT development in wild-type mice and greatly potentiated in mice with genetic deletion of Bscl2 in brown progenitor cells, leading to reduced BAT mass and lipid content during neonatal brown fat formation. However, prolonged overactivation of cAMP/PKA signaling during BAT development ultimately causes apoptosis of brown adipocytes through inflammation, resulting in BAT atrophy and increased overall adiposity in adult mice. These findings reveal a key cell-autonomous role for BSCL2 in controlling BAT mass/activity and provide novel insights into therapeutic strategies targeting cAMP/PKA signaling to regulate brown adipocyte function, viability, and metabolic homeostasis.
    Note
    6 Month Embargo.
    ISSN
    0270-7306
    1098-5549
    DOI
    10.1128/MCB.01120-15
    Version
    Final published version
    Sponsors
    American Heart Association (AHA) [12SDG9080000]; HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) [HL112640, HL132182, HL126949]
    Additional Links
    http://mcb.asm.org/lookup/doi/10.1128/MCB.01120-15
    ae974a485f413a2113503eed53cd6c53
    10.1128/MCB.01120-15
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    UA Faculty Publications

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