Katsunori Nonogaki

TL;DR: Findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus.

TL;DR: It is shown that young adult mice with a targeted mutation of the serotonin 5-HT2C receptor gene consume more food despite normal responses to exogenous leptin administration, demonstrating a dissociation of serotonin and leptin signaling in the regulation of feeding and indicating that a perturbation of brain serotonin systems can predispose to type 2 diabetes.

TL;DR: It is demonstrated that changes in hepatic triglyceride metabolism are another acute phase response that can be induced by IL-6, and the hypertriglyceridemia induced byIL-6 was due to increased secretion by the liver.

TL;DR: The results suggest that the effects of PPAR-gamma activators on lipid metabolism and energy homeostasis in obesity and type 2 diabetes may be partly mediated through their effects on PPAR -gamma in the liver.

TL;DR: Findings provide a mechanistic explanation for the longstanding observation of HPA axis stimulation in response to 5-HT and thereby give insight into the neural circuitry mediating the complex neuroendocrine responses to stress.