@article{HoffmannEbertHankiretal.2021,
  author    = {Hoffmann, Annett and Ebert, Thomas and Hankir, Mohammed K. and Flehmig, Gesine and Kl{\"o}ting, Nora and Jessnitzer, Beate and L{\"o}ssner, Ulrike and Stumvoll, Michael and Bl{\"u}her, Matthias and Fasshauer, Mathias and T{\"o}njes, Anke and Miehle, Konstanze and Kralisch, Susan},
  title     = {Leptin improves parameters of brown adipose tissue thermogenesis in lipodystrophic mice},
  series = {Nutrients},
  volume    = {13},
  journal   = {Nutrients},
  number    = {8},
  issn      = {2072-6643},
  doi       = {10.3390/nu13082499},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-242787},
  year      = {2021},
  abstract  = {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.},
  language  = {en}
}
@article{HankirRotzingerNordbecketal.2021,
  author    = {Hankir, Mohammed K. and Rotzinger, Laura and Nordbeck, Arno and Corteville, Caroline and Dischinger, Ulrich and Knop, Juna-Lisa and Hoffmann, Annett and Otto, Christoph and Seyfried, Florian},
  title     = {Leptin receptors are not required for Roux-en-Y gastric bypass surgery to normalize energy and glucose homeostasis in rats},
  series = {Nutrients},
  volume    = {13},
  journal   = {Nutrients},
  number    = {5},
  issn      = {2072-6643},
  doi       = {10.3390/nu13051544},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-239550},
  year      = {2021},
  abstract  = {Sensitization to the adipokine leptin is a promising therapeutic strategy against obesity and its comorbidities and has been proposed to contribute to the lasting metabolic benefits of Roux-en-Y gastric bypass (RYGB) surgery. We formally tested this idea using Zucker fatty fa/fa rats as an established genetic model of obesity, glucose intolerance, and fatty liver due to leptin receptor deficiency. We show that the changes in body weight in these rats following RYGB largely overlaps with that of diet-induced obese Wistar rats with intact leptin receptors. Further, food intake and oral glucose tolerance were normalized in RYGB-treated Zucker fatty fa/fa rats to the levels of lean Zucker fatty fa/+ controls, in association with increased glucagon-like peptide 1 (GLP-1) and insulin release. In contrast, while fatty liver was also normalized in RYGB-treated Zucker fatty fa/fa rats, their circulating levels of the liver enzyme alanine aminotransferase (ALT) remained elevated at the level of obese Zucker fatty fa/fa controls. These findings suggest that the leptin system is not required for the normalization of energy and glucose homeostasis associated with RYGB, but that its potential contribution to the improvements in liver health postoperatively merits further investigation.},
  language  = {en}
}