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    The brown adipose tissue glucagon receptor is functional but not essential for control of energy homeostasis in mice

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    1-s2.0-S2212877819300419-main.pdf
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    Author
    Beaudry, Jacqueline L
    Kaur, Kiran Deep
    Varin, Elodie M
    Baggio, Laurie L
    Cao, Xiemin
    Mulvihill, Erin E
    Stern, Jennifer H
    Campbell, Jonathan E
    Scherer, Phillip E
    Drucker, Daniel J
    Affiliation
    Univ Arizona, Coll Med, Div Endocrinol
    Issue Date
    2019-04
    Keywords
    Adiposity
    Energy expenditure
    Glucagon
    Lipolysis
    Thermogenesis
    brown adipose tissue
    
    Metadata
    Show full item record
    Publisher
    ELSEVIER SCIENCE BV
    Citation
    Beaudry, J. L., Kaur, K. D., Varin, E. M., Baggio, L. L., Cao, X., Mulvihill, E. E., ... & Drucker, D. J. (2019). The brown adipose tissue glucagon receptor is functional but not essential for control of energy homeostasis in mice. Molecular metabolism, 22, 37-48.
    Journal
    MOLECULAR METABOLISM
    Rights
    © 2019 The Authors. Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license.
    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
    Objective: Administration of glucagon (GCG) or GCG-containing co-agonists reduces body weight and increases energy expenditure. These actions appear to be transduced by multiple direct and indirect GCG receptor (GCGR)-dependent mechanisms. Although the canonical GCGR is expressed in brown adipose tissue (BAT) the importance of BAT GCGR activity for the physiological control of body weight, or the response to GCG agonism, has not been defined. Methods: We studied the mechanisms linking GCG action to acute increases in oxygen consumption using wildtype (WT), Ucp1(-/-) and Fgf21(-/-) mice. The importance of basal GCGR expression within the Myf5(+) domain for control of body weight, adiposity, glucose and lipid metabolism, food intake, and energy expenditure was examined in Gcgr(BAT-/-) mice housed at room temperature or 4 degrees C, fed a regular chow diet (RCD) or after a prolonged exposure to high fat diet (HFD). Results: Acute GCG administration induced lipolysis and increased the expression of thermogenic genes in BAT cells, whereas knockdown of Gcgr reduced expression of genes related to thermogenesis. GCG increased energy expenditure (measured by oxygen consumption) both in vivo in WT mice and ex vivo in BAT and liver explants. GCG also increased acute energy expenditure in Ucp1(-/-) mice, but these actions were partially blunted in Ffg21(-/-) mice. However, acute GCG administration also robustly increased oxygen consumption in Gcgr(BAT-/-) mice. Moreover, body weight, glycemia, lipid metabolism, body temperature, food intake, activity, energy expenditure and adipose tissue gene expression profiles were normal in Gcgr(BAT-/-) mice, either on RCD or HFD, whether studied at room temperature, or chronically housed at 4 degrees C. Conclusions: Exogenous GCG increases oxygen consumption in mice, also evident both in liver and BAT explants ex vivo, through UCP1-independent, FGF21-dependent pathways. Nevertheless, GCGR signaling within BAT is not physiologically essential for control of body weight, whole body energy expenditure, glucose homeostasis, or the adaptive metabolic response to cold or prolonged exposure to an energy dense diet. (C) 2019 The Authors. Published by Elsevier GmbH.
    Note
    Open access journal
    ISSN
    2212-8778
    PubMed ID
    30772257
    DOI
    10.1016/j.molmet.2019.01.011
    Version
    Final published version
    Sponsors
    Diabetes Canada; Canadian Diabetes Association; Canadian Institutes of Health Research; Banting and Best Diabetes Centre, University of Toronto; US National Institutes of Health (NIH) [R00AG055649, R01-DK55758, P01-DK088761, R01-DK099110, P01-AG051459]; Novo Nordisk Research Foundation; Banting and Best Diabetes Centre-Novo Nordisk Chair in Incretin Biology; Canadian Institutes of Health Research [154321]; Novo Nordisk Inc.
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.molmet.2019.01.011
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