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.

瘦素是一种众所周知的食欲激素，在包括脂肪，肝脏和肌肉组织在内的周围组织的脂肪代谢中发挥作用。在这项研究中，我们调查了源自棕色海藻Ishige okamurae的Ishophloroglucin A的抗肥胖和脂肪堆积调节作用，它通过瘦素信号通路在高脂饮食诱导的肥胖小鼠模型的外周组织中发挥作用。通过给C57BL / 6J小鼠喂高脂饮食10周来诱导肥胖，并在最后4周内口服Ishophloroglucin A（2.5 mg / kg）进行肥胖治疗。在实验期间，每周监测一次体重。实验后，使用商业试剂盒测量了几种血清生化参数，并使用免疫组织化学方法观察了白色脂肪，肝脏和肌肉组织。Ishophloroglucinin A可显着降低谷氨酸草酰乙酸转氨酶，谷氨酸丙酮酸转氨酶和瘦素水平，这些都是由于高脂饮食而增加的。另外，Ishophloroglucin A可以在所有检查的周围组织中明显激活瘦素信号传导途径，减少脂肪组织的大小，并减轻肝脏和肌肉组织的脂肪变性。这些结果表明，Ishophloroglucin A治疗4周可积极诱导与瘦素信号传导有关的分子机制和组织学改变。这些发现表明，在高脂饮食诱导的肥胖小鼠中，恒定的Ishophloroglucin A治疗通过瘦素信号传导途径明显调节肥胖和外周脂肪积累。