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 - TY - JOUR A1 - Kaya-Zeeb, Sinan A1 - Delac, Saskia A1 - Wolf, Lena A1 - Marante, Ana Luiza A1 - Scherf-Clavel, Oliver A1 - Thamm, Markus T1 - Robustness of the honeybee neuro-muscular octopaminergic system in the face of cold stress JF - Frontiers in Physiology N2 - In recent decades, our planet has undergone dramatic environmental changes resulting in the loss of numerous species. This contrasts with species that can adapt quickly to rapidly changing ambient conditions, which require physiological plasticity and must occur rapidly. The Western honeybee (Apis mellifera) apparently meets this challenge with remarkable success, as this species is adapted to numerous climates, resulting in an almost worldwide distribution. Here, coordinated individual thermoregulatory activities ensure survival at the colony level and thus the transmission of genetic material. Recently, we showed that shivering thermogenesis, which is critical for honeybee thermoregulation, depends on octopamine signaling. In this study, we tested the hypothesis that the thoracic neuro-muscular octopaminergic system strives for a steady-state equilibrium under cold stress to maintain endogenous thermogenesis. We can show that this applies for both, octopamine provision by flight muscle innervating neurons and octopamine receptor expression in the flight muscles. Additionally, we discovered alternative splicing for AmOARβ2. At least the expression of one isoform is needed to survive cold stress conditions. We assume that the thoracic neuro-muscular octopaminergic system is finely tuned in order to contribute decisively to survival in a changing environment. KW - honeybees KW - thermogenesis KW - cold stress KW - octopamine KW - octopamine receptors KW - gene expression Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-288753 SN - 1664-042X VL - 13 ER - TY - JOUR A1 - Kaya-Zeeb, Sinan A1 - Engelmayer, Lorenz A1 - Straßburger, Mara A1 - Bayer, Jasmin A1 - Bähre, Heike A1 - Seifert, Roland A1 - Scherf-Clavel, Oliver A1 - Thamm, Markus T1 - Octopamine drives honeybee thermogenesis JF - eLife N2 - In times of environmental change species have two options to survive: they either relocate to a new habitat or they adapt to the altered environment. Adaptation requires physiological plasticity and provides a selection benefit. In this regard, the Western honeybee (Apis mellifera) protrudes with its thermoregulatory capabilities, which enables a nearly worldwide distribution. Especially in the cold, shivering thermogenesis enables foraging as well as proper brood development and thus survival. In this study, we present octopamine signaling as a neurochemical prerequisite for honeybee thermogenesis: we were able to induce hypothermia by depleting octopamine in the flight muscles. Additionally, we could restore the ability to increase body temperature by administering octopamine. Thus, we conclude that octopamine signaling in the flight muscles is necessary for thermogenesis. Moreover, we show that these effects are mediated by β octopamine receptors. The significance of our results is highlighted by the fact the respective receptor genes underlie enormous selective pressure due to adaptation to cold climates. Finally, octopamine signaling in the service of thermogenesis might be a key strategy to survive in a changing environment. KW - honeybee KW - octopamine KW - thermogenesis Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-301327 VL - 11 ER -