首页> 美国卫生研究院文献>Marine Drugs >Chitosan Oligosaccharide Alleviates Abnormal Glucose Metabolism without Inhibition of Hepatic Lipid Accumulation in a High-Fat Diet/Streptozotocin-Induced Diabetic Rat Model
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Chitosan Oligosaccharide Alleviates Abnormal Glucose Metabolism without Inhibition of Hepatic Lipid Accumulation in a High-Fat Diet/Streptozotocin-Induced Diabetic Rat Model

机译:壳聚糖寡糖可减轻异常的葡萄糖代谢而不抑制高脂饮食/链脲佐菌素诱导的糖尿病大鼠模型中的肝脂肪积累

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摘要

This study investigated the effects of chitosan oligosaccharide (COS) on glucose metabolism and hepatic steatosis in a high-fat (HF) diet/streptozotocin-induced diabetic rat model. Male Wistar rats were divided into: (1) normal control (NC group), (2) HF diet (HF group), (3) streptozotocin (STZ)-induced diabetes with HF diet (DF group), and DF group supplemented with (4) 0.5% COS (D0.5F group), (5) 1% COS (D1F group), and (6) 5% COS (D5F group) for 4 weeks. COS supplementation significantly decreased the plasma glucose, BUN, creatinine, uric acid, triglyceride (TG), and total cholesterol (TC) levels, and hepatic glucose-6-phosphatase activity, and significantly increased hepatic hexokinase activity and glycogen content in diabetic rats; but the increased hepatic TG and TC levels could not be significantly decreased by COS supplementation. Supplementation of COS increased superoxide dismutase activity and decreased lipid peroxidation products in the diabetic rat livers. COS supplementation significantly increased phosphorylated AMP-activated protein kinase (AMPK) protein expression, and attenuated protein expression of hepatic phosphoenolpyruvate carboxykinase (PEPCK) and phosphorylated p38 and renal sodium-glucose cotransporter-2 (SGLT2) in diabetic rats. These results suggest that COS may possess a potential for alleviating abnormal glucose metabolism in diabetic rats through the inhibition of hepatic gluconeogenesis and lipid peroxidation and renal SGLT2 expression.
机译:本研究研究了壳聚糖寡糖(COS)对高脂(HF)饮食/链脲佐菌素诱导的糖尿病大鼠模型中葡萄糖寡糖(COS)对葡萄糖代谢和肝脏脂肪变性的影响。雄性Wistar大鼠分为:(1)正常对照(NC组),(2)HF饮食(HF组),(3)链脲佐菌素(STZ)诱导患有HF饮食(DF组)的糖尿病和补充的DF组(4)0.5%COS(D0.5F组),(5)1%COS(D1F组),和(6)5%COS(D5F组)4周。 COS补充显着降低了血浆葡萄糖,面包,肌酐,尿酸,甘油三酯(Tg)和总胆固醇(Tc)水平,以及糖尿病大鼠中的肝六酮酶活性和糖原含量显着增加的肝葡萄糖-6-磷酸酶活性。但COS补充不能显着降低增加的肝TG和TC水平。加强超氧化物歧化酶活性和糖尿病大鼠肝脏中脂质过氧化产物的补充。 COS补充显着增加了磷酸化的AMP活化蛋白激酶(AMPK)蛋白表达和肝磷酸丙烯酸羧酮糖蛋白酶(PEPCK)和磷酸化的P38和肾脏钠 - 葡萄糖COTRANSPORTER-2(SGLT2)的催化蛋白表达。这些结果表明,COS可以通过抑制肝葡糖苷生成和脂质过氧化和肾脏SGLT2表达来抑制糖尿病大鼠中的异常葡萄糖代谢的潜力。

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