Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
Diabetes Care. 2013 Jul;36(7):1919-25. doi: 10.2337/dc12-1912. Epub 2013 Feb 12.
To study the effects of high-protein versus high-carbohydrate diets on various metabolic end points (glucoregulation, oxidative stress [dichlorofluorescein], lipid peroxidation [malondialdehyde], proinflammatory cytokines [tumor necrosis factor-α and interleukin-6], adipokines, and resting energy expenditure [REE]) with high protein-low carbohydrate (HP) and high carbohydrate-low protein (HC) diets at baseline and after 6 months of dietary intervention.
We recruited obese, premenopausal women aged 20-50 years with no diabetes or prediabetes who were randomized to HC (55% carbohydrates, 30% fat, and 15% protein) or HP (40% carbohydrates, 30% fat, and 30% protein) diets for 6 months. The diets were provided in prepackaged food, which provided 500 kcal restrictions per day. The above metabolic end points were measured with HP and HC diet at baseline and after 6 months of dietary intervention.
After 6 months of the HP versus HC diet (12 in each group), the following changes were significantly different by Wilcoxon rank sum test for the following parameters: dichlorofluorescein (-0.8 vs. -0.3 µmol/L, P < 0.0001), malondialdehyde (-0.4 vs. -0.2 μmol/L, P = 0.0004), C-reactive protein (-2.1 vs. -0.8 mg/L, P = 0.0003), E-selectin (-8.6 vs. -3.7 ng/mL, P = 0.0007), adiponectin (1,284 vs. 504 ng/mL, P = 0.0011), tumor necrosis factor-α (-1.8 vs. -0.9 pg/mL, P < 0.0001), IL-6 (-1.3 vs. -0.4 pg/mL, P < 0.0001), free fatty acid (-0.12 vs. 0.16 mmol/L, P = 0.0002), REE (259 vs. 26 kcal, P < 0.0001), insulin sensitivity (4 vs. 0.9, P < 0.0001), and β-cell function (7.4 vs. 2.1, P < 0.0001).
To our knowledge, this is the first report on the significant advantages of a 6-month hypocaloric HP diet versus hypocaloric HC diet on markers of β-cell function, oxidative stress, lipid peroxidation, proinflammatory cytokines, and adipokines in normal, obese females without diabetes.
研究高蛋白与高碳水化合物饮食对各种代谢终点（血糖调节、氧化应激[二氯荧光素]、脂质过氧化[丙二醛]、促炎细胞因子[肿瘤坏死因子-α和白细胞介素-6]、脂肪因子和静息能量消耗[REE]）的影响，基线和 6 个月饮食干预后采用高蛋白质-低碳水化合物（HP）和高碳水化合物-低蛋白质（HC）饮食。
我们招募了肥胖、绝经前、年龄在 20-50 岁、无糖尿病或糖尿病前期的女性，将其随机分为 HC（55%碳水化合物、30%脂肪和 15%蛋白质）或 HP（40%碳水化合物、30%脂肪和 30%蛋白质）饮食组，干预时间为 6 个月。饮食以预包装食品形式提供，每天限制摄入 500 卡路里。在基线和 6 个月的饮食干预后，使用 HP 和 HC 饮食测量上述代谢终点。
在 HP 与 HC 饮食（每组 12 人）6 个月后，Wilcoxon 秩和检验显示以下参数的变化有显著差异：二氯荧光素（-0.8 对-0.3 μmol/L，P<0.0001）、丙二醛（-0.4 对-0.2 μmol/L，P=0.0004）、C 反应蛋白（-2.1 对-0.8 mg/L，P=0.0003）、E-选择素（-8.6 对-3.7 ng/mL，P=0.0007）、脂联素（1284 对 504 ng/mL，P=0.0011）、肿瘤坏死因子-α（-1.8 对-0.9 pg/mL，P<0.0001）、白细胞介素-6（-1.3 对-0.4 pg/mL，P<0.0001）、游离脂肪酸（-0.12 对 0.16 mmol/L，P=0.0002）、REE（259 对 26 kcal，P<0.0001）、胰岛素敏感性（4 对 0.9，P<0.0001）和β细胞功能（7.4 对 2.1，P<0.0001）。
据我们所知，这是首次报道 6 个月低热量 HP 饮食相对于低热量 HC 饮食对正常肥胖、无糖尿病女性的β细胞功能、氧化应激、脂质过氧化、促炎细胞因子和脂肪因子标志物的显著优势。
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