首页> 美国卫生研究院文献>Nutrients >Melatonin Improves Fatty Liver Syndrome by Inhibiting the Lipogenesis Pathway in Hamsters with High-Fat Diet-Induced Hyperlipidemia
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Melatonin Improves Fatty Liver Syndrome by Inhibiting the Lipogenesis Pathway in Hamsters with High-Fat Diet-Induced Hyperlipidemia

机译:褪黑素通过抑制高脂饮食诱发的高脂血症仓鼠的脂肪生成途径来改善脂肪肝综合征。

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摘要

The aim of this study was to investigate the effect of melatonin on hepatic lipid metabolism in hamsters with high-fat diet (HFD)-induced dyslipidemia. Male Syrian hamsters were kept on either a chow control (C) or HFD for four weeks. After four weeks, animals fed the HFD were further randomly assigned to four groups: high-fat only (P), melatonin low-dosage (L), medium-dosage (M), and high-dosage (H) groups. The L, M, and H groups, respectively, received 10, 20, and 50 mg/kg/day of a melatonin solution, while the P and C groups received the ethanol vehicle. After eight weeks of the intervention, results showed that a low dose of melatonin significantly reduced HFD-induced hepatic cholesterol and triglycerides; decreased plasma cholesterol, triglycerides, and low-density lipoprotein cholesterol; and increased plasma high-density lipoprotein cholesterol (p < 0.05). In addition, melatonin markedly decreased activities of the hepatic lipogenic enzymes, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) (p < 0.05), and elevated the relative hepatic carnitine palmitoyltransferase-1α expression in hamsters with HFD-induced hyperlipidemia. Consequently, melatonin reduced activities of the hepatic lipogenic enzymes, ACC and FAS. In summary, chronic melatonin administration improved HFD-induced dyslipidemia and hepatic lipid accumulation in Syrian hamsters with HFD-induced dyslipidemia, which might have occurred through inhibiting the lipogenesis pathway.
机译:这项研究的目的是研究褪黑激素对高脂饮食(HFD)引起的血脂异常的仓鼠肝脂质代谢的影响。将叙利亚雄性仓鼠放在食物对照(C)或HFD上四个星期。四周后,将喂食HFD的动物进一步随机分为四组:仅高脂(P),褪黑激素低剂量(L),中剂量(M)和高剂量(H)组。 L,M和H组分别接受10、20和50 mg / kg /天的褪黑激素溶液,而P和C组接受乙醇媒介物。干预八周后,结果表明,低剂量的褪黑激素可显着降低HFD诱导的肝胆固醇和甘油三酸酯;降低血浆胆固醇,甘油三酸酯和低密度脂蛋白胆固醇;血浆高密度脂蛋白胆固醇升高(p <0.05)。此外,褪黑素显着降低了具有HFD诱导的高脂血症的仓鼠的肝脏脂肪生成酶,乙酰辅酶A羧化酶(ACC)和脂肪酸合酶(FAS)的活性(p <0.05),并提高了相对于肝脏肉碱棕榈酸转移酶-1α的表达。 。因此,褪黑激素降低了肝脂肪酶,ACC和FAS的活性。总之,长期服用褪黑激素可以改善HFD引起的血脂异常的叙利亚仓鼠中HFD引起的血脂异常和肝脂质蓄积,这可能是通过抑制脂肪生成途径而发生的。

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