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Li, Y.* ; Schnabl, K.* ; Gabler, S.M.* ; Willershäuser, M.* ; Reber, J. ; Karlas, A. ; Laurila, S.* ; Lahesmaa, M.* ; U Din, M.* ; Bast-Habersbrunner, A.* ; Virtanen, K.A.* ; Fromme, T.* ; Bolze, F.* ; O'Farrell, L.S.* ; Alsina-Fernandez, J.* ; Coskun, T.* ; Ntziachristos, V. ; Nuutila, P.* ; Klingenspor, M.*

Secretin-activated brown fat mediates prandial thermogenesis to induce satiation.

Cell 175, 1561-1574 (2018)
Open Access Green as soon as Postprint is submitted to ZB.
The molecular mediator and functional significance of meal-assosiated brown fat (BAT) thermogenesis remains elusive. Here, we identified the gut hormone secretin as a non-synmpathetic BAT activator mediating prandial thermogenesis, which consequentially induces satiation, thereby establishing a gut-secretin-BAT-brain axis in mammals with a physiological role of prandial thermogenesis in the control of satiation. Mechanistically, meal-associated rise in circulating secretin activates BAT thermogenesis by stimulating lipolysis upon binding to secretin receptors in brown adipocytes, is sensed in the brain and promotes satiation. Chronic infusion of a modified human secretin transiently elevates energy expenditure in diet-induced obese mice. Clinical trials with human subjects showed that thermogenesis after a single-meal ingestion correlated with postprandial secretin levels and that secretin infusions increased glucose uptake in BAT. Collectively, our findings highlight the largely unappreciated function of BAT in the control of satiation and qualify BAT as an even more attractive target for treating obesity.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Ucp1 ; Energy Balance ; Gut Hormone ; Heat ; Inter-organ Communication ; Metabolism ; Satiation ; Secretin ; Secretin Receptor ; Thermogenesis; Adipose-tissue Thermogenesis; Food-intake; Cold-acclimation; Gastrointestinal Hormones; Insulin Sensitivity; Energy-expenditure; Glucose; Meal; Adipocytes; Humans
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Journal Cell
Quellenangaben Volume: 175, Issue: 6, Pages: 1561-1574 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Mass.
Reviewing status Peer reviewed