Ishophloroglucin A, derived from Ishige okamurae, regulates high-fat-diet-induced fat accumulation via the leptin signaling pathway, associated with peripheral metabolism

Abstract Leptin, a well-known appetite hormone, plays a role in fat metabolism in peripheral tissues including the adipose, liver, and muscle tissues. In this study, we investigated the antiobesity and fat accumulation regulatory effects of Ishophloroglucin A, derived from the brown seaweed Ishige okamurae, which acts via the leptin signaling pathway in the peripheral tissues of a high-fat-diet-induced obese mouse model. Obesity in C57BL/6J mice was induced by feeding them with a high-fat diet for 10 weeks and Ishophloroglucin A (2.5 mg/kg) was orally treated for the last 4 weeks. Body weights were monitored once per week during the experimental period. After the experiment, several serum biochemical parameters were measured using commercial kits and the white adipose, liver, and muscle tissues were observed using immunohistochemistry methods. Ishophloroglucin A significantly reduced glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and leptin level, which increase as a result of high-fat diet. Also, Ishophloroglucin A clearly activated the leptin signaling pathway in all examined peripheral tissues, reduced the adipose tissue size, and alleviated steatosis in the liver and muscle tissues. These results implied that Ishophloroglucin A treatment for 4 weeks positively induced molecular mechanisms and histologic changes related with leptin signaling. These findings suggested that constant Ishophloroglucin A treatment clearly regulates obesity and peripheral fat accumulation via the leptin signaling pathway in high-fat-diet-induced obese mice.