Relationship of dietary fat and serum cholesterol ester and phospholipid fatty acids to markers of insulin resistance in men and women with a range of glucose tolerance
Relationship of dietary fat and serum cholesterol ester and phospholipid fatty acids to markers of insulin resistance in men and women with a range of glucose tolerance
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DOI：
10.1053/meta.2001.19440
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发表时间：
2001-01-01
影响因子：
9.8
通讯作者：
Rood, JC
中科院分区：
文献类型：
--
作者：
Lovejoy, JC;Champagne, CM;Rood, JC
高脂肪饮食与胰岛素抵抗有关，然而，这种影响可能因摄入的脂肪类型而异。本研究的目的是在口服葡萄糖耐量试验（OGTT）期间确定特定膳食脂肪酸的摄入量（通过3天饮食记录和血清胆固醇酯（CEs）和磷脂（PLs）的脂肪酸组成来评估）与葡萄糖和胰岛素浓度之间的关系。19名男性和19名女性完成了这项研究。9名受试者患有2型糖尿病或糖耐量受损。血浆胰岛素与总脂肪（r = 0.50, P < 0.01）、单不饱和脂肪（r = 0.44, P < 0.01）和饱和脂肪（r = 0.49, P < 0.01）的摄入相关，但与反式脂肪酸摄入无关（r = 0.11，无统计学意义[NS]）。糊状葡萄糖也与总脂肪摄入量（r = 0.49, P < 0.05）和单不饱和脂肪摄入量（r = 0.37, P < 0.05）相关。在多变量分析中，总脂肪和饱和脂肪摄入量都是空腹胰岛素（R-2）的单一预测因子。25)，一个结合饮食和人体测量的模型占空腹胰岛素方差的47%。空腹胰岛素与肉豆蔻酸（C14:0）、棕榈油酸（C16:1）和二同γ -亚麻酸（C20:3n-6）血清CE浓度之间存在显著关系。在多变量分析中，一个包含CE 14:0和体脂百分比的模型解释了45%的空腹胰岛素方差，C14:0和年龄解释了30%的空腹血糖方差。PL C20:3n-6解释了30%的空腹胰岛素差异，包含PL C18:1n-11 cis、C20:3n-6、年龄和体脂的模型的R2为0.58。总之，自我报告摄入饱和脂肪和单不饱和脂肪，而非反式脂肪酸，与胰岛素抵抗标志物有关。此外，血清CE和PI中二同γ -亚麻酸和肉豆蔻酸的增加可能是饮食摄入的标记物，预测胰岛素抵抗。W.B. Saunders Company版权所有(C) 2001。
High-fat diets are associated with insulin resistance, however, this effect may vary depending on the type of fat consumed. The purpose of this study was to determine the relationship between intakes of specific dietary fatty acids (assessed by 3-day diet records and fatty acid composition of serum cholesterol esters [CEs] and phospholipids [PLs]) and glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Nineteen men and 19 women completed the study. Nine subjects had type 2 diabetes or impaired glucose tolerance. Pasting insulin correlated with reported intakes of total fat (r = .50, P < .01), monounsaturated fat (r = .44, P < .01), and saturated fat (r = .49, P < .01), but not with trans fatty acid intake (r = .11, not significant [NS]). Pasting glucose also correlated with total (r = .49, P < .05) and monounsaturated fat intakes (r = .37, P < .05). In multivariate analysis, both total and saturated fat intake were strong single predictors of fasting insulin (R-2 .25), and a model combining dietary and anthropometric measures accounted for 47% of the variance in fasting insulin. Significant relationships were observed between fasting insulin and the serum CE enrichments of myristic (C14:0), palmitoleic (C16:1), and dihomo-gamma -linolenic (C20:3n-6) acids. In multivariate analysis, a model containing CE 14:0 and percent body fat explained 45% of the variance in fasting insulin, and C14:0 and age explained 30% of the variance in fasting glucose. PL C20:3n-6 explained 30% of the variance in fasting insulin, and a model including PL C18:1n-11 cis, C20:3n-6, age and body fat had an R2 of .58. In conclusion, self-reported intake of saturated and monounsaturated fats, but not trans fatty acids, are associated with markers of insulin resistance. Furthermore, enhancement of dihomo-gamma -linolenic and myristic acids in serum CE and PI presumably markers for dietary intake, predicted insulin resistance. Copyright (C) 2001 by W.B. Saunders Company.