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Hoffmann, A.L.* ; Ebert, T.* ; Hankir, M.K.* ; Flehmig, G.* ; Klöting, N. ; Jessnitzer, B.* ; Lössner, U.* ; Stumvoll, M.* ; Blüher, M. ; Fasshauer, M.* ; Tönjes, A.* ; Miehle, K.* ; Kralisch, S.*

Leptin improves parameters of brown adipose tissue thermogenesis in lipodystrophic mice.

Nutrients 13:2499 (2021)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Lipodystrophy syndromes (LD) are a heterogeneous group of very rare congenital or acquired disorders characterized by a generalized or partial lack of adipose tissue. They are strongly associated with severe metabolic dysfunction due to ectopic fat accumulation in the liver and other organs and the dysregulation of several key adipokines, including leptin. Treatment with leptin or its analogues is therefore sufficient to reverse some of the metabolic symptoms of LD in patients and in mouse models through distinct mechanisms. Brown adipose tissue (BAT) thermogenesis has emerged as an important regulator of systemic metabolism in rodents and in humans, but it is poorly understood how leptin impacts BAT in LD. Here, we show in transgenic C57Bl/6 mice overexpressing sterol regulatory element-binding protein 1c in adipose tissue (Tg (aP2-nSREBP1c)), an established model of congenital LD, that daily subcutaneous administration of 3 mg/kg leptin for 6 to 8 weeks increases body temperature without affecting food intake or body weight. This is associated with increased protein expression of the thermogenic molecule uncoupling protein 1 (UCP1) and the sympathetic nerve marker tyrosine hydroxylase (TH) in BAT. These findings suggest that leptin treatment in LD stimulates BAT thermogenesis through sympathetic nerves, which might contribute to some of its metabolic benefits by providing a healthy reservoir for excess circulating nutrients.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Brown Adipose Tissue ; Leptin ; Lipodystrophy ; Sympathetic Nervous System ; Thermogenesis ; Uncoupling Protein 1; Insulin-resistance; Diabetes-mellitus; Hepatic Steatosis; Body-temperature; Sensitivity; Mechanisms; Therapy; Model; Cold
ISSN (print) / ISBN 2072-6643
e-ISSN 2072-6643
Zeitschrift Nutrients
Quellenangaben Band: 13, Heft: 8, Seiten: , Artikelnummer: 2499 Supplement: ,
Verlag MDPI
Verlagsort Basel
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen EFSD Mentorship Programme - AstraZeneca
University Leipzig, Medical Faculty
Deutsche Diabetes Gesellschaft
HI-MAG
Deutsche Forschungsgemeinschaft (DFG, German Research foundation)
Nachwuchsforderprogramm of the Medical Faculty, University of Leipzig
Projektpreis der AG Diabetes und Niere 2020 by the Deutsche Diabetes Gesellschaft
Novo Nordisk postdoctoral fellowship
Karolinska Institutet, Stockholm, Sweden
Njurfonden (Swedish Kidney Foundation)
Stiftelsen Stig och Gunborg Westman
Karolinska Institutet Research Foundation grant