PuSH - Publikationsserver des Helmholtz Zentrums München: Celastrol-induced weight loss is driven by hypophagia and independent from UCP1.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Pfuhlmann, K. ; Schriever, S.C. ; Baumann, P. ; Kabra, D.G.* ; Harrison, L. ; Mazibuko-Mbeje, S. ; Contreras, R.E.* ; Kyriakou, E. ; Simonds, S.E.* ; Tiganis, T.* ; Cowley, M.A.* ; Woods, S.C.* ; Jastroch, M. ; Clemmensen, C. ; de Angelis, M. ; Schramm, K.-W. ; Sattler, M. ; Messias, A.C. ; Tschöp, M.H. ; Pfluger, P.T.

Celastrol-induced weight loss is driven by hypophagia and independent from UCP1.

Diabetes 67, 2456-2465 (2018)

Verlagsversion

Postprint

Forschungsdaten

DOI

PMC

	Open Access Green

Abstract
Metriken
Zusatzinfos

Celastrol, a plant-derived constituent of traditional Chinese medicine, has been proposed to offer significant potential as an antiobesity drug. However, the molecular mechanism for this activity is unknown. We show that the weight-lowering effects of celastrol are driven by decreased food consumption. Although young Lep(ob) mice respond with a decrease in food intake and body weight, adult Lep(db) and Lep(ob) mice are unresponsive to celastrol, suggesting that functional leptin signaling in adult mice is required to elicit celastrol's catabolic actions. Protein tyrosine phosphatase 1 (PTP1B), a leptin negative-feedback regulator, has been previously reported to be one of celastrol's targets. However, we found that global PTP1B knockout (KO) and wild-type (WT) mice have comparable weight loss and hypophagia when treated with celastrol. Increased levels of uncoupling protein 1 (UCP1) in subcutaneous white and brown adipose tissue suggest celastrol-induced thermogenesis as a further mechanism. However, diet-induced obese UCP1 WT and KO mice have comparable weight loss upon celastrol treatment, and celastrol treatment has no effect on energy expenditure under ambient housing or thermoneutral conditions. Overall, our results suggest that celastrol-induced weight loss is hypophagia driven and age-dependently mediated by functional leptin signaling. Our data encourage reconsideration of therapeutic antiobesity strategies built on leptin sensitization.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

7.273

1.868