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首页> 美国卫生研究院文献>Marine Drugs >Anti-Obesity Effect of Chitosan Oligosaccharide Capsules (COSCs) in Obese Rats by Ameliorating Leptin Resistance and Adipogenesis
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Anti-Obesity Effect of Chitosan Oligosaccharide Capsules (COSCs) in Obese Rats by Ameliorating Leptin Resistance and Adipogenesis

机译：壳聚糖寡糖胶囊（COSCs）通过改善瘦素抵抗力和成脂作用对肥胖大鼠的抗肥胖作用

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Obesity is a global disease that causes many metabolic disorders. However, effective agents for the prevention or treatment of obesity remain limited. This study investigated the anti-obesity effect and mechanism of chitosan oligosaccharide capsules (COSCs) on rats suffering from obesity induced by a high-fat diet (HFD). After the eight-week administration of COSCs on obese rats, the body weight gain, fat/body ratio, and related biochemical indices were measured. The hepatic expressions of the leptin signal pathway (JAK2-STAT3) and gene expressions of adipogenesis-related targets were also determined. Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.
机译：肥胖症是一种全球性疾病，会引起许多代谢紊乱。但是，用于预防或治疗肥胖的有效药物仍然有限。这项研究调查了壳聚糖寡糖胶囊（COSCs）对高脂饮食（HFD）诱导的肥胖大鼠的抗肥胖作用及其机理。在肥胖大鼠上服用COSC八周后，测量了体重增加，脂肪/体比以及相关的生化指标。还确定了瘦素信号途径（JAK2-STAT3）的肝表达和脂肪形成相关靶标的基因表达。我们的数据表明，COSC可以调节体重增加，脂质，血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶，并上调肝瘦素受体b（LepRb）以及JAK2和STAT3的磷酸化。同时，肝固醇调节元件结合蛋白-1c，脂肪酸合酶，乙酰辅酶A羧化酶，3-羟基-3-甲基戊二酰辅酶A还原酶，脂联素，脂肪过氧化物酶体增殖物激活受体γ，CCAAT增强剂的表达明显增加。观察到蛋白质α，脂肪分化相关蛋白质和SREBP-1c。结果表明COSCs激活JAK2-STAT3信号通路来减轻瘦素抵抗并抑制脂肪生成以减少脂质积累。因此，它们可以潜在地用于肥胖症治疗。

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