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低碳水化合物饮食与常规饮食在肥胖症中引起的脂肪细胞因子变化的比较。

Adipocytokine changes caused by low-carbohydrate compared to conventional diets in obesity.

机构信息

Division of Endocrinology, Department of Medicine, University of Pennsylvania Medical School, Philadelphia, Pennsylvania., Department of Medicine, Veterans Affairs Medical Center, Philadelphia, Pennsylvania.

出版信息

Metab Syndr Relat Disord. 2005;3(1):66-74. doi: 10.1089/met.2005.3.66.

DOI:10.1089/met.2005.3.66
PMID:18370712
Abstract

Modest weight loss causing a decrease in insulin resistance has been linked to favorable changes in the adipocyte cytokines leptin, adiponectin, and tumor necrosis factor-alpha (TNF-alpha), three emerging risk factors of cardiovascular disease. We previously observed a significant reduction in insulin resistance with weight loss in obese subjects on a low-carbohydrate diet. Based on these previous findings, we hypothesize that a low-carbohydrate diet would be more beneficial in changing leptin, TNF-alpha, and adiponectin than a conventional diet. A total of 75 severely obese (body mass index >/=35 kg/m(2)) subjects were randomized to instruction of 6 months of a low-carbohydrate diet or a conventional calorie-restricted diet. Serum levels of leptin, TNF-alpha, TNF-alpha-soluble receptor 1 (TNF-alpha SR1), and adiponectin were measured at baseline and after 6 months of dietary intervention. Subjects on low-carbohydrate diets experienced a greater decrease in leptin when compared to conventional dieters (p < 0.001). TNF-alpha increased significantly in nondiabetic subjects on conventional vs. low-carbohydrate diets (p = 0.003). Adiponectin and TNF-alpha SR1 change were not significantly different between diets. This is the first study to report the effects of dietary macronutrient alterations on serum adipocytokines in a randomized controlled trial. The greater reduction in insulin resistance and weight on a low-carbohydrate diet, in the short term, translates into greater improvement in leptin but with no significant improvements in TNF-alpha or adiponectin in patients with moderate to severe obesity after 6 months of dietary intervention.

摘要

适度的体重减轻导致胰岛素抵抗降低与脂肪细胞细胞因子瘦素、脂联素和肿瘤坏死因子-α(TNF-α)的有利变化有关,这三种细胞因子是心血管疾病的新出现的风险因素。我们之前观察到,肥胖患者在低碳水化合物饮食下体重减轻时,胰岛素抵抗显著降低。基于这些先前的发现,我们假设低碳水化合物饮食在改变瘦素、TNF-α和脂联素方面比传统饮食更有益。共有 75 名严重肥胖(体重指数>/=35 kg/m(2)) 受试者被随机分配到 6 个月的低碳水化合物饮食或传统热量限制饮食的指导下。在基线和 6 个月的饮食干预后测量血清瘦素、TNF-α、TNF-α可溶性受体 1(TNF-α SR1)和脂联素水平。与传统节食者相比,低碳水化合物饮食者的瘦素水平下降幅度更大(p < 0.001)。在非糖尿病患者中,常规饮食与低碳水化合物饮食相比,TNF-α显著增加(p = 0.003)。饮食之间脂联素和 TNF-α SR1 的变化没有显著差异。这是第一项在随机对照试验中报告饮食宏量营养素改变对血清脂肪细胞因子影响的研究。短期内,低碳水化合物饮食在减轻体重和胰岛素抵抗方面的更大改善,导致瘦素水平的更大改善,但在 6 个月的饮食干预后,中度至重度肥胖患者的 TNF-α或脂联素没有显著改善。

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