TrpC5 Mediates Acute Leptin and Serotonin Effects via Pomc Neurons

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The molecular mechanisms underlying acute leptin and serotonin 2C receptor-induced hypophagia remain unclear. Here, we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is sufficient to decrease energy expenditure and increase food intake resulting in elevated body weight. Deficiency of Trpc5 subunits in Pomc neurons is also sufficient to block the anorexigenic effects of leptin and serotonin 2C receptor (Ht2Cr) agonists. The loss of acute anorexigenic effects of these receptors is concomitant with a blunted electrophysiological response to both leptin and Ht2Cr agonists in arcuate Pomc neurons. We also demonstrate that the Ht2Cr agonist lorcaserin-induced improvements in glucose and insulin tolerance are blocked by TrpC5 deficiency in Pomc neurons. Together, our results link TrpC5 subunits in the brain with leptinand serotonin 2C receptor-dependent changes in neuronal activity, as well as energy balance, feeding behavior, and glucose metabolism.
Publisher
CELL PRESS
Issue Date
2017-01
Language
English
Article Type
Article
Keywords

HYPOTHALAMIC PROOPIOMELANOCORTIN NEURONS; REGULATES GLUCOSE-HOMEOSTASIS; ARCUATE NUCLEUS; ENERGY-BALANCE; AGRP NEURONS; INSULIN SENSITIVITY; FEEDING CIRCUITS; NEUROPEPTIDE-Y; D-FENFLURAMINE; BODY-WEIGHT

Citation

CELL REPORTS, v.18, no.3, pp.583 - 592

ISSN
2211-1247
DOI
10.1016/j.celrep.2016.12.072
URI
http://hdl.handle.net/10203/220920
Appears in Collection
BS-Journal Papers(저널논문)
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