Nesfatin-1 is involved in hyperbaric oxygen-mediated therapeutic effects in high fat diet-induced hyperphagia in mice.

Obesity is a worldwide health issue. Effective and safe methods for obesity management are highly desirable. In the current study, hyperbaric oxygen (HBO) treatment was investigated as a potential treatment against obesity-associated hyperphagia and hyperenergy intake. Diet induced obesity (DIO) mice model was established with high fat diet (HFD) feeding, HBO was then co-administered. Food and energy intake were assessed with nocturnal food intake assay. Immunohistochemistry for c-Fos was performed for neuronal activation in arcuate nucleus (ARC), paraventricular nucleus of hypothalamus (PVN) and lateral parabrachial nucleus (LPBN) of brain. Additionally, enzyme-linked immunosorbent assay (ELISA) in serum and immunofluorescence in LPBN were performed. Results indicated that HBO co-treatment effectively decreased food and energy intake in DIO mice, reverted the abnormal neuronal activation in the ARC and PVN, and enhanced both peripheral and central nesfatin-1 peptide levels without affecting serum leptin levels. While SHU9119 microinjection in LPBN effectively abolished the beneficial effects of HBO on body weight, visceral fat, nocturnal feeding and energy intake in DIO mice. In conclusion, HBO treatment could effectively protect against HFD-induced increase of food and energy intake, which is associated with its central effects against abnormal neuronal activation in ARC and PVN and enhanced peptide levels of nesfatin-1 both centrally and peripherally. The melanocortin system downstream of nesfatin-1 may exert a potential effect in this process.