Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet
Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet
复制标题
DOI：
10.1016/s0026-0495(98)90331-6
复制
发表时间：
1998-10-01
影响因子：
9.8
通讯作者：
Dornhorst, A
中科院分区：
文献类型：
--
作者：
Frost, G;Leeds, A;Dornhorst, A
冠心病（CHD）的风险受到家族史、胰岛素敏感性（IS）和饮食的影响。肥胖影响CHD和IS。IS的细胞机制被认为涉及脂肪细胞因子肿瘤坏死因子-α（TNF-α）。在61名绝经前妇女中测定了胰岛素刺激的皮下和网膜脂肪细胞的葡萄糖摄取，这些脂肪细胞是在择期手术中获得的，其中24名有冠心病病史。在体内IS测量使用短胰岛素耐量试验（SITT）在28名妇女，16 PH-CHD，之前和3周后随机分配到低血糖指数（LGI）或高血糖指数（HGI）的饮食。在体外脂肪细胞IS和TNF-α的生产进行了测量后，饮食的修改。在习惯性饮食中，体外胰岛素刺激的脂肪细胞葡萄糖摄取在基础水平上的百分比增加在PH-CHD女性中比没有PH-CHD的女性少（以中位数表示，95%置信限：皮下，28%（17%至39%）vs 96%）（70%至120%），P <0.01）;网膜，40%（28%至52%）vs113%（83%至143%），P <0.01）。在饮食随机化之前，16名PH-CHD受试者和12名对照者的体内IS相似，并且在摄入LGI与HGI饮食的两组中均增加（PH-CHD，0.31（0.26至0.37）v 0.14（0.10至0.24）mmol/L/min，P <0.01;对照组，0.31（0.1至0.53）v 0.15（0.06至0.23）mmol/L/min，P <0.05）。采用LGI饮食的PH-CHD女性的脂肪细胞IS高于采用HGI饮食的PH-CHD女性（皮下，50%（20%至98%）vs13%（1%至29%）;网膜，97%（47%至184%）vs29%（4%至84%），P <0.05）。有PH-CHD的女性脂肪细胞TNF-α的产生高于无PH-CHD的女性（皮下，0.3（0.18 ~ 0.42）v0.93（0.39 ~ 1.30）ng/mL/min;内脏，0.22（0.15 ~ 1.30）v0.64（0.24 ~ 1.1）ng/mL/min，P <0.04），但不受饮食血糖指数的影响。我们的结论是，在体外脂肪细胞IS减少和脂肪细胞TNF-α的生产增加绝经前妇女与PH-CHD。LGI饮食改善了PH-CHD女性的脂肪细胞IS以及PH-CHD女性和非PH-CHD女性的体内IS。版权所有（C）1998由W.B.桑德斯公司
The risk of coronary heart disease (CHD) is influenced by family history, insulin sensitivity (IS), and diet. Adiposity affects CHD and IS. The cellular mechanism of IS is thought to involve the adipocyte cytokine tumor necrosis factor-alpha (TNF-alpha). Insulin-stimulated glucose uptake in isolated subcutaneous and omental adipocytes obtained during elective surgery was measured in 61 premenopausal women, 24 with a parental history (PH) of CHD. In vivo IS was measured using the short insulin tolerance test (SITT) in 28 women, 16 with PH-CHD, before and 3 weeks after randomization to a low glycemic index (LGI) or high glycemic index (HGI) diet. In vitro adipocyte IS and TNF-alpha production was measured following dietary modification. On the habitual diet, in vitro insulin-stimulated glucose uptake in adipocytes as a percentage increase over basal was less in women with PH-CHD than in those without it (presented as the median with 95% confidence limits: subcutaneous, 28% (17% to 39%) v 96% (70% to 120%), P < .01); omental, 40% (28% to 52%) v 113% (83% to 143%), P < .01). In vivo IS in 16 PH-CHD subjects and 12 controls before dietary randomization was similar, and increased in both groups consuming a LGI versus HGI diet (PH-CHD, 0.31 (0.26 to 0.37) v 0.14 (0.10 to 0.24) mmol/L/min, P < .01; controls, 0.31 (0.1 to 0.53) v 0.15 (0.06 to 0.23) mmol/l/min, P < .05). Adipocyte IS was greater in PH-CHD women on a LGI versus HGI diet (subcutaneous, 50% (20% to 98%) v 13% (1% to 29%); omental, 97% (47% to 184%) v 29% (4% to 84%), P < .05). Adipocyte TNF-alpha production was higher in women with versus without PH-CHD (subcutaneous, 0.3 (0.18 to 0.42) v 0.93 (0.39 to 1.30) ng/mL/min; visceral, 0.22 (0.15 to 1.30) v 0.64 (0.24 to 1.1) ng/mL/min, P < .04, respectively), but was uninfluenced by the dietary glycemic index. We conclude that in vitro adipocyte IS is reduced and adipocyte TNF-alpha production is increased in premenopausal women with PH-CHD. A LGI diet improves both adipocyte IS in women with PH-CHD and in vivo IS in women with and without PH-CHD. Copyright (C) 1998 by W.B. Saunders Company.