[1] Increased nesfatin-1 in the hypothalamus contributes to diminished hunger, a 'sense of fullness', and a potential loss of body fat and weight.
A study of metabolic effects of nesfatin-1 in rats was done in which subjects administered nesfatin-1 ate less, used more stored fat and became more active.
[4] Nesfatin-1 is expressed in the hypothalamus, in other areas of the brain, and in pancreatic islets, gastric endocrine cells and adipocytes.
In addition, it is proposed that feeding-activated nesfatin-1 neurons in the PVN and SON could play an important role in the postprandial regulation of feeding behavior and energy homeostasis.
[8] There is growing evidence that nesfatin-1 may play an important role in the regulation of food intake and glucose homeostasis.
[9] For instance, continuous infusion of nesfatin-1 into the third brain ventricle significantly decreased food intake and body weight gain in rats.
In addition, suppression of HGP by central nesfatin-1 was dependent on an inhibition of the substrate flux through G-6-Pase and not on a decrease in the amount of G-6-Pase enzyme.
In this study, we demonstrate that central nesfatin-1 resulted in increased phosphorylation of AMPK accompanied by a marked suppression of hepatic PEPCK activity, mRNA, and protein levels in both SD and HFD rats.
We found that central nesfatin-1 produced a pronounced increase in insulin-mediated phosphorylation of Akt in the liver of HFD-fed rats.
This provided correlative evidence that Akt activation may be involved in nesfatin-1 signaling and its effects on glucose homeostasis and insulin sensitivity.
To gain further insight into the mechanism underlying the insulin-sensitizing effects of ICV nesfatin-1, we assessed mTOR and TORC2 phosphorylation in liver samples of SD- and HFD-fed animals.
Thus, it's postulated that the mTOR/TORC2 plays a role as a negative-feedback mechanism in the regulation of metabolism and insulin sensitivity mediated by central nesfatin-1.