Horm Metab Res 2019; 51(10): 678-685
DOI: 10.1055/a-0985-4272
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

Nesfatin-1 Acts Centrally to Induce Sympathetic Activation of Brown Adipose Tissue and Non-Shivering Thermogenesis

Luka Levata
1   Department of Internal Medicine I, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
Riccardo Dore
1   Department of Internal Medicine I, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
Olaf Jöhren
2   Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
Markus Schwaninger
3   Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
Carla Schulz*
1   Department of Internal Medicine I, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
Hendrik Lehnert*
1   Department of Internal Medicine I, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany
› Author Affiliations
Further Information

Publication History

received 05 March 2019

accepted 23 July 2019

Publication Date:
05 September 2019 (online)


Nesfatin-1 has originally been established as a bioactive peptide interacting with key hypothalamic nuclei and neural circuitries in control of feeding behavior, while its effect on energy expenditure has only recently been investigated. Hence, the aim of this study was to examine whether centrally acting nesfatin-1 can induce β3-adrenergic stimulation, which is a prerequisite for the activation of thermogenic genes and heat release from interscapular brown adipose tissue, key physiological features that underlie increased energy expenditure. This question was addressed in non-fasted mice stereotactically cannulated to receive nesfatin-1 intracerebroventricularly together with peripheral injection of the β3-adrenoceptor antagonist SR 59230 A, to assess whole-body energy metabolism. Using a minimally invasive thermography technique, we now demonstrate that the thermogenic effect of an anorectic nesfatin-1 dose critically depends on β3 adrenergic stimulation, as the co-administration with SR 59230 A completely abolished heat production from interscapular brown adipose tissue and rise in ocular surface temperature, thus preventing body weight loss. Moreover, through indirect calorimetry it could be shown that the anorectic concentration of nesfatin-1 augments overall caloric expenditure. Plausibly, central administration of nesfatin-1 also enhanced the expression of DIO2 and CIDEA mRNA in brown adipose tissue critically involved in the regulation of thermogenesis.

* These authors share senior authorship.

Supplementary Material

  • References

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