Premium
Nesfatin‐1 increases energy expenditure and reduces food intake in rats
Author(s) -
Wernecke Kerstin,
Lamprecht Ingolf,
Jöhren Olaf,
Lehnert Hendrik,
Schulz Carla
Publication year - 2014
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20736
Subject(s) - thermogenesis , leptin , endocrinology , medicine , neuropeptide y receptor , adipokine , hypothalamus , energy homeostasis , energy expenditure , food intake , brown adipose tissue , central nervous system , homeostasis , neuropeptide , adipose tissue , obesity , receptor
Objective Energy homeostasis results from a balance of food intake and energy expenditure, accomplished by the interaction of peripheral and central nervous signals. The recently discovered adipokine nesfatin‐1 is involved in the central control of food intake, but whether it also participates in the regulation of thermogenesis is unknown. Methods Nesfatin‐1 was administered intracerebroventricularly to freely moving, male Wistar rats and direct calorimetry was performed to assess its effects on thermogenesis. Furthermore, food intake was measured and hypothalamic and N. tractus solitarius (NTS) neuropeptide expression was determined by quantitative real‐time polymerace chain reaction. Leptin, which is involved in both the regulation of food intake and thermogenesis, was used as positive control. Results For the first time it was shown that central nervous administration of nesfatin‐1 profoundly increases thermogenesis in rats to a similar extent as leptin and the role of both peptides in the control of food intake was confirmed. Nesfatin‐1 significantly downregulated neuropeptide Y (NPY) mRNA expression in both hypothalamus and NTS. Conclusions The results strongly support the prominent role of nesfatin‐1 for both energy expenditure and food intake and NPY neurons appear to be involved in this effect.