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肥胖受试者中肝素后脂蛋白脂肪酶活性的营养调节

Nutrient regulation of post-heparin lipoprotein lipase activity in obese subjects.

作者信息

Ranganath L R, Beety J M, Wright J, Morgan L M

机构信息

Department of Chemical Pathology, Epsom General Hospital, Surrey, UK.

出版信息

Horm Metab Res. 2001 Jan;33(1):57-61. doi: 10.1055/s-2001-12628.

Abstract

This study examines the immediate effect of ingestion of oral carbohydrate and fat on lipoprotein lipase (LPL) activity post-heparin in six lean and six obese age-matched women. Subjects were given, on two separate occasions, 340 kcal carbohydrate or an equicaloric amount of fat, both in 300 ml of water. Post-heparin LPL activity (10,000 U) was measured on each occasion 120 minutes after ingestion of the meal. Following oral carbohydrate postprandial plasma insulin levels were significantly higher in obese subjects than in lean (p < 0.01). Impaired glucose tolerance was seen in the obese group. GIP secretion was similar in lean and obese subjects both during oral fat and carbohydrate ingestion. GLP-1 secretion post-carbohydrate was lower in obese subjects. Total LPL activity unadjusted for body weight was similar in the two groups after carbohydrate administration but was significantly lower when adjusted per kg body weight. Total LPL activity was lower in the lean group at 130 minutes after fat administration (p < 0.02). Fasting serum triglycerides were higher in the obese group and were inversely related to the post-carbohydrate LPL activity (r = - 0.65, p < 0.02). Intraluminal lipoprotein lipase activity is not increased in established obesity. Fat and carbohydrate nutrients may affect LPL activity differently in lean and obese subjects.

摘要

本研究调查了在6名体重正常且年龄匹配的女性和6名肥胖女性中,口服碳水化合物和脂肪对肝素后脂蛋白脂肪酶(LPL)活性的即时影响。在两个不同的时间段,受试者分别摄入340千卡碳水化合物或等量脂肪,均溶于300毫升水中。在摄入餐后120分钟,每次都测量肝素后LPL活性(10,000单位)。口服碳水化合物后,肥胖受试者餐后血浆胰岛素水平显著高于体重正常者(p < 0.01)。肥胖组出现葡萄糖耐量受损。在口服脂肪和碳水化合物期间,体重正常和肥胖受试者的GIP分泌相似。肥胖受试者碳水化合物摄入后的GLP-1分泌较低。给予碳水化合物后,两组未根据体重调整的总LPL活性相似,但按每千克体重调整后,肥胖组显著更低。给予脂肪后130分钟,体重正常组的总LPL活性较低(p < 0.02)。肥胖组空腹血清甘油三酯较高,且与碳水化合物摄入后的LPL活性呈负相关(r = - 0.65,p < 0.02)。在已确诊的肥胖症中,管腔内脂蛋白脂肪酶活性并未增加。脂肪和碳水化合物营养素对体重正常和肥胖受试者LPL活性的影响可能不同。

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