Endocannabinoid regulation in white and brown adipose tissue following thermogenic activation
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Endocannabinoid regulation in white and brown adipose tissue following thermogenic activation. / Krott, Lucia M; Piscitelli, Fabiana; Heine, Markus; Borrino, Simona; Scheja, Ludger; Silvestri, Cristoforo; Heeren, Joerg; Di Marzo, Vincenzo.
In: J LIPID RES, Vol. 57, No. 3, 03.2016, p. 464-73.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Endocannabinoid regulation in white and brown adipose tissue following thermogenic activation
AU - Krott, Lucia M
AU - Piscitelli, Fabiana
AU - Heine, Markus
AU - Borrino, Simona
AU - Scheja, Ludger
AU - Silvestri, Cristoforo
AU - Heeren, Joerg
AU - Di Marzo, Vincenzo
N1 - Copyright © 2016 by the American Society for Biochemistry and Molecular Biology, Inc.
PY - 2016/3
Y1 - 2016/3
N2 - The endocannabinoids and their main receptor, cannabinoid type-1 (CB1), suppress intracellular cyclic AMP levels and have emerged as key players in the control of energy metabolism. CB1 agonists and blockers have been reported to influence the thermogenic function of white and brown adipose tissue (WAT and BAT), affecting body weight through the inhibition and stimulation of energy expenditure, respectively. The purpose of the current study was to investigate the regulation of the endocannabinoid system in WAT and BAT following exposure to either cold or specific agonism of β3-adrenoceptors using CL316,243 (CL), conditions known to cause BAT activation and WAT browning. To address this question, we performed quantitative PCR-based mRNA profiling of genes important for endocannabinoid synthesis, degradation, and signaling, and determined endocannabinoid levels by LC-MS in WAT and BAT of control, cold-exposed, and CL-treated wild-type mice as well as primary brown adipocytes. Treatment with CL and exposure to cold caused an upregulation of endocannabinoid levels and biosynthetic enzymes in WAT. Acute β3-adrenoceptor activation increased endocannabinoids and a subset of genes of biosynthesis in BAT and primary brown adipocytes. We suggest that the cold-mediated increase in endocannabinoid tone is part of autocrine negative feed-back mechanisms controlling β3-adrenoceptor-induced BAT activation and WAT browning.
AB - The endocannabinoids and their main receptor, cannabinoid type-1 (CB1), suppress intracellular cyclic AMP levels and have emerged as key players in the control of energy metabolism. CB1 agonists and blockers have been reported to influence the thermogenic function of white and brown adipose tissue (WAT and BAT), affecting body weight through the inhibition and stimulation of energy expenditure, respectively. The purpose of the current study was to investigate the regulation of the endocannabinoid system in WAT and BAT following exposure to either cold or specific agonism of β3-adrenoceptors using CL316,243 (CL), conditions known to cause BAT activation and WAT browning. To address this question, we performed quantitative PCR-based mRNA profiling of genes important for endocannabinoid synthesis, degradation, and signaling, and determined endocannabinoid levels by LC-MS in WAT and BAT of control, cold-exposed, and CL-treated wild-type mice as well as primary brown adipocytes. Treatment with CL and exposure to cold caused an upregulation of endocannabinoid levels and biosynthetic enzymes in WAT. Acute β3-adrenoceptor activation increased endocannabinoids and a subset of genes of biosynthesis in BAT and primary brown adipocytes. We suggest that the cold-mediated increase in endocannabinoid tone is part of autocrine negative feed-back mechanisms controlling β3-adrenoceptor-induced BAT activation and WAT browning.
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1194/jlr.M065227
DO - 10.1194/jlr.M065227
M3 - SCORING: Journal article
C2 - 26768656
VL - 57
SP - 464
EP - 473
JO - J LIPID RES
JF - J LIPID RES
SN - 0022-2275
IS - 3
ER -
