首页> 美国卫生研究院文献>Journal of Clinical Medicine >Lysosomal Acid Lipase as a Molecular Target of the Very Low Carbohydrate Ketogenic Diet in Morbidly Obese Patients: The Potential Effects on Liver Steatosis and Cardiovascular Risk Factors
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Lysosomal Acid Lipase as a Molecular Target of the Very Low Carbohydrate Ketogenic Diet in Morbidly Obese Patients: The Potential Effects on Liver Steatosis and Cardiovascular Risk Factors

机译:溶酶体酸性脂肪酶作为病态肥胖患者极低碳水化合物生酮饮食的分子靶标:对肝脂肪变性和心血管危险因素的潜在影响

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摘要

A very low carbohydrate ketogenic diet (VLCKD) is an emerging technique to induce a significant, well-tolerated, and rapid loss of body weight in morbidly obese patients. The low activity of lysosomal acid lipase (LAL) could be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), which is a common feature in morbidly obese patients. Fifty-two obese patients suitable for a bariatric surgery intervention underwent a 25-day-long VLCKD. The biochemical markers of glucose and lipid metabolism, and flow-mediated dilation (FMD) of the brachial artery were measured before and after VLCKD. LAL activity was measured using the dried blood spot technique in 20 obese patients and in a control group of 20 healthy, normal-weight subjects. After VLCKD, we observed a significant reduction in body mass index, fasting glucose, insulinemia, and lipid profile parameters. No significant variation in FMD was observed. The number of patients with severe liver steatosis significantly decreased. LAL activity significantly increased, although the levels were not significantly different as compared to the control group. In conclusion, VLCKD induces the activity of LAL in morbidly obese subjects and reduces the secretion of all circulating lipoproteins. These effects could be attributed to the peculiar composition of the diet, which is particularly poor in carbohydrates and relatively rich in proteins.
机译:极低的碳水化合物生酮饮食(VLCKD)是一种新兴技术,可以在病态肥胖患者中诱导明显的,良好的耐受性和快速的体重减轻。溶酶体酸性脂肪酶(LAL)的低活性可能与非酒精性脂肪肝(NAFLD)的发病机制有关,这是病态肥胖患者的常见特征。 52名适合进行减肥手术的肥胖患者接受了为期25天的VLCKD。在VLCKD之前和之后,测量了葡萄糖和脂质代谢的生化标志物,以及肱动脉的血流介导的扩张(FMD)。使用干血斑技术在20例肥胖患者和20例健康,体重正常的对照组中测量LAL活性。 VLCKD后,我们观察到体重指数,空腹血糖,胰岛素血症和脂质谱参数显着降低。没有观察到FMD的显着变化。严重肝脂肪变性的患者人数明显减少。 LAL活性显着增加,尽管与对照组相比水平没有显着差异。总之,VLCKD可以诱导病态肥胖受试者的LAL活性,并减少所有循环脂蛋白的分泌。这些影响可以归因于饮食的特殊组成,其碳水化合物特别少,蛋白质相对丰富。

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