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Swim exercise training ameliorates hepatocyte ultrastructural alterations in rats fed on a high fat and sugar diet

机译:游泳运动训练改善了在高脂肪和糖饮食中喂养的大鼠的肝细胞超微结构改变

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Excessive consumption of carbohydrate and fat increases the risk of liver disease. We hypothesized that swim exercise can protect hepatocytes from ultra-structural damage induced by high cholesterol and fructose diets (HCFD). Rats were either fed with HCFD (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. Swim exercise trained rats started the treatment from the 11th week until the sacrifice day, end of week 15. Blood samples were assayed for biomarkers of liver injury and adiponectin. The harvested liver tissues were examined using transmission electron microscopy (TEM). TEM images revealed substantial damage and accumulation of lipid droplets (steatosis) in the hepatocytes of the model group that was inhibited by swim exercise. In addition, HCFD significantly (p < 0.0005) increased insulin resistance index (HOMA-IR), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), which were effectively (p < 0.02) decreased by a swim exercise to levels comparable to control group. Whereas, swim exercise increased adiponectin levels in HCFD group (p < 0.03). These results show that HCFD-induced hepatic injury is ameliorated by swim training exercise possibly via restoration of a normal blood sugar and lipid, induction of adiponectin and inhibition of inflammatory, and liver injury biomarkers.
机译:过量消耗碳水化合物和脂肪会增加肝病的风险。我们假设游泳运动可以保护高胆固醇和果糖饮食(HCFD)引起的超结构损伤免受肝细胞。在处死前15周,用HCFD(模型组)或标准实验室食物(对照组)喂食大鼠。游泳运动培训的大鼠从第11周开始治疗,直到牺牲日,第15周结束。测定血液样品的肝损伤和脂联素的生物标志物。使用透射电子显微镜(TEM)检查收获的肝组织。 TEM图像揭示了游泳运动抑制的模型组肝细胞中脂液滴(脂肪变性)的大量损伤和积累。此外,HCFD显着(P <0.0005)增加了胰岛素抵抗指数(HOMA-IR),白细胞介素-6(IL-6),肿瘤坏死因子-α(TNF-A),丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶( AST)有效(P <0.02)通过游泳运动减少到与对照组相当的水平。虽然,游泳运动增加了HCFD组的脂联素水平(P <0.03)。这些结果表明,HCFD诱导的肝损伤是通过恢复正常血糖和脂质,诱导脂联素和炎症和肝损伤生物标志物的抑制和肝损伤生物标志物的水分训练运动来改善。

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