TY  - JOUR
A1  - Hoffmann, Annett
A1  - Ebert, Thomas
A1  - Hankir, Mohammed K.
A1  - Flehmig, Gesine
A1  - Klöting, Nora
A1  - Jessnitzer, Beate
A1  - Lössner, Ulrike
A1  - Stumvoll, Michael
A1  - Blüher, Matthias
A1  - Fasshauer, Mathias
A1  - Tönjes, Anke
A1  - Miehle, Konstanze
A1  - Kralisch, Susan
T1  - Leptin improves parameters of brown adipose tissue thermogenesis in lipodystrophic mice
JF  - Nutrients
N2  - 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.
KW  - lipodystrophy
KW  - leptin
KW  - brown adipose tissue
KW  - thermogenesis
KW  - uncoupling protein 1
KW  - sympathetic nervous system
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-242787
SN  - 2072-6643
VL  - 13
IS  - 8
ER  -