YNCRG Inhibited Metabolic Syndrome Through Appetite Suppression and Improved Lipid Metabolism in Metabolic Syndrome Model Rats

Abstract

Increased body fat mass can lead to lifestyle diseases such as hypertension, diabetes, and hyperlipidemia. Metabolic syndrome is a cluster of conditions that increases the onset of multiple diseases, such as cardiovascular diseases, stroke, and type 2 diabetes, which are closely related to lipid metabolism; therefore, new prevention approaches and treatments are needed. Our study investigated the effects and mechanism of YNCRG on anti-obesity in metabolic syndrome model SHR.Cg-Leprcp/NDmcr (SHRCP) rats. Eight-week-old male SHRCP rats were administered YNCRG or water by gavage for eight weeks and sacrificed. The tissues were immediately dissected for future experiments. We also used WKY rats as a rodent model. YNCRG induced reductions in food intake, body weight, and body fat mass in SHRCP rats. We also analyzed the mechanism of food intake regulation in the hypothalamus. Expression of POMC was significantly increased in the YNCRG group. However, JAK2 showed no change between the two groups. Phosphorylation levels of Akt (Ser473) and FoxO1 were significantly increased in the YNCRG group. Moreover, mTOR was significantly phosphorylated by YNCRG treatment. These results suggest that YNCRG can induce appetite suppression through the mTOR-Akt-FoxO1-POMC signaling pathway. YNCRG also induced a reduction in body fat mass. In adipose tissue, phosphorylation of AMPK was significantly increased in the YNCRG group. Also, LKB1 and PKA (upstream factors of AMPK), and ACC and HSL (downstream factors of AMPK) were significantly phosphorylated with the YNCRG treatment. Our results indicate that YNCRG can treat MetS by decreasing body fat mass of SHRCP rats through appetite suppression and improvement of lipid metabolism.