WKYMVm ameliorates obesity by improving lipid metabolism and leptin signalling

Obesity is a metabolic disorder that results from an imbalance of energy intake and consumption. As low-grade chronic inflammation caused by obesity can lead to various complications, it is important to develop effective treatments against obesity. In this study, we investigate the effects of WKYMVm, a strong anti-inflammatory agent, against obesity. Administration of WKYMVm into high fat diet (HFD)-induced obese mice significantly attenuated body weight gain, food intake and increased insulin sensitivity. HFD-induced hepatic steatosis and adipose tissue hypertrophy were also markedly ameliorated by WKYMVm. During the maturation of adipocytes, WKYMVm improves lipid metabolism by increasing lipolysis, adipogenesis, mitochondrial biogenesis and fat browning. WKYMVm administration also elicited a decrease in leptin levels, but an increase in leptin sensitivity via regulation of hypothalamic endoplasmic reticulum stress and the leptin receptor cascade. Taken together, our results show that WKYMVm ameliorates obesity by improving lipid metabolism and leptin signalling, suggesting that WKYMVm can be a useful molecule for the development of anti-obesity agents.

Automated summary

Obesity is a metabolic disorder caused by an imbalance of energy intake and consumption, and its chronic inflammation can lead to various complications. This study investigates the effects of WKYMVm, an anti-inflammatory agent, against obesity. The results show that WKYMVm attenuates body weight gain, improves insulin sensitivity, ameliorates hepatic steatosis and adipose tissue hypertrophy induced by a high fat diet. WKYMVm also improves lipid metabolism and leptin signaling, suggesting its potential as an anti-obesity agent.