School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China.
Guangdong Engineering Research Center of Natural Products and New Drugs, Guangdong Provincial University Engineering Technology Research Center of Natural Products and Drugs, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Mar Drugs. 2018 Jun 5;16(6):198. doi: 10.3390/md16060198.
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.
肥胖是一种全球性疾病,可导致许多代谢紊乱。然而,用于预防或治疗肥胖的有效药物仍然有限。本研究探讨了壳寡糖胶囊(COSCs)对高脂肪饮食(HFD)诱导肥胖大鼠的抗肥胖作用及其机制。在肥胖大鼠给予 COSC 八周后,测量体重增加、脂肪/体重比和相关生化指标。还测定了肝瘦素信号通路(JAK2-STAT3)的表达和脂肪生成相关靶基因的表达。我们的数据表明,COSCs 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)和 JAK2 和 STAT3 的磷酸化。同时,观察到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-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 增强子结合蛋白 α、脂肪分化相关蛋白和 SREBP-1c 的表达明显增加。结果表明,COSCs 通过激活 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,它们可能可用于肥胖症的治疗。