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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)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Zeitschrift Cell
Quellenangaben Band: 175, Heft: 6, Seiten: 1561-1574 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed