Paniagua J A, Gallego de la Sacristana A, Romero I, Vidal-Puig A, Latre J M, Sanchez E, Perez-Martinez P, Lopez-Miranda J, Perez-Jimenez F
Lipids and Atherosclerosis Research Unit, Reina Sofía University Hospital, Córdoba, Spain.
Diabetes Care. 2007 Jul;30(7):1717-23. doi: 10.2337/dc06-2220. Epub 2007 Mar 23.
Central obesity is associated with insulin resistance through factors that are not fully understood. We studied the effects of three different isocaloric diets on body fat distribution, insulin sensitivity, and peripheral adiponectin gene expression.
Eleven volunteers, offspring of obese type 2 diabetic patients with abdominal fat deposition, were studied. These subjects were considered insulin resistant as indicated by Matsuda index values <4 after an oral glucose tolerance test, and they maintained A1C <6.5% without therapeutic intervention. All subjects underwent three dietary periods of 28 days each in a crossover design: 1) diet enriched in saturated fat (SAT), 2) diet rich in monounsaturated fat (MUFA) (Mediterranean diet), and 3) diet rich in carbohydrates (CHOs).
Weight, body composition, and resting energy expenditure remained unchanged during the three sequential dietary periods. Using dual-energy X-ray absorptiometry we observed that when patients were fed a CHO-enriched diet, their fat mass was redistributed toward the abdominal depot, whereas periphery fat accumulation decreased compared with isocaloric MUFA-rich and high-SAT diets (ANOVA P < 0.05). Changes in fat deposition were associated with decreased postprandial mRNA adiponectin levels in peripheral adipose tissue and lower insulin sensitivity index values from a frequently sampled insulin-assisted intravenous glucose tolerance test in patients fed a CHO-rich diet compared with a MUFA-rich diet (ANOVA P < 0.05).
An isocaloric MUFA-rich diet prevents central fat redistribution and the postprandial decrease in peripheral adiponectin gene expression and insulin resistance induced by a CHO-rich diet in insulin-resistant subjects.
中心性肥胖通过一些尚未完全明确的因素与胰岛素抵抗相关。我们研究了三种不同的等热量饮食对身体脂肪分布、胰岛素敏感性和外周脂联素基因表达的影响。
对11名志愿者进行了研究,这些志愿者均为患有腹部脂肪沉积的肥胖2型糖尿病患者的后代。口服葡萄糖耐量试验后,根据松田指数值<4表明这些受试者存在胰岛素抵抗,且在无治疗干预的情况下他们的糖化血红蛋白(A1C)<6.5%。所有受试者采用交叉设计,各进行三个为期28天的饮食阶段:1)富含饱和脂肪(SAT)的饮食,2)富含单不饱和脂肪(MUFA)的饮食(地中海饮食),3)富含碳水化合物(CHO)的饮食。
在三个连续的饮食阶段中,体重、身体成分和静息能量消耗均保持不变。使用双能X线吸收法,我们观察到,当患者食用富含CHO的饮食时,他们的脂肪量会重新分布到腹部储存部位,而与等热量的富含MUFA和高SAT的饮食相比,外周脂肪堆积减少(方差分析P<0.05)。脂肪沉积的变化与外周脂肪组织中餐后脂联素mRNA水平降低以及与食用富含MUFA饮食的患者相比,食用富含CHO饮食的患者在频繁采样胰岛素辅助静脉葡萄糖耐量试验中较低的胰岛素敏感性指数值相关(方差分析P<0.05)。
在胰岛素抵抗的受试者中,等热量的富含MUFA的饮食可防止中心性脂肪重新分布以及富含CHO的饮食所诱导的餐后外周脂联素基因表达降低和胰岛素抵抗。