Effect of an acute hyperinsulinaemic clamp on post-prandial lipaemia in subjects with insulin resistance.
Effect of an acute hyperinsulinaemic clamp on post-prandial lipaemia in subjects with insulin resistance.
复制标题
急性高胰岛素钳夹对胰岛素抵抗受试者餐后血脂的影响。
DOI：
10.1111/j.1365-2362.2006.01651.x
复制
发表时间：
2006
影响因子：
5.5
通讯作者：
Mamo,JCL
中科院分区：
文献类型：
--
作者：
Allister,EM;James,AP;Watts,GF;Barrett,PHR;Mamo,JCL
背景肥胖、胰岛素抵抗个体的肠道和肝脏脂蛋白水平升高。胰岛素降低生产的肝脂蛋白in vivo andso本研究旨在探讨是否急性高胰岛素血症，正常血钳夹可以纠正空腹和餐后血脂dyslipidaemia.Subjects and methodsIn一项随机，交叉设计，餐后血脂进行了比较，无论是与胰岛素输注，以达到稳态浓度为100 mU L-1或与生理盐水。9名肥胖（体重指数> 26 kg m−2;腰臀比> 1.0）胰岛素抵抗（稳态模型评估评分> 2.0）男性受试者在输注开始后3 h接受口服脂肪负荷，并继续采样6 h。血浆载脂蛋白B-48，甘油三酯和非酯化脂肪酸（NEFA）每小时测定。结果平均稳态血清胰岛素水平在高胰岛素钳夹过程中为123 ± 4·4 mU L-1。配对分析显示，当以（apoB-48）增量曲线下面积（IAUC）计算时，胰岛素对餐后乳糜微粒代谢无净效应。然而，apoB-48峰值有延迟的趋势，与乳糜微粒生物生成、脂解和/或清除率的可能变化一致。同样，输注胰岛素或生理盐水的受试者的餐后脂血症（描述为甘油三酯IAUC）相似，但胰岛素输注期间餐后反应峰值延迟。NEFA迅速下降了83%，3小时后的胰岛素infrations.ConclusionsIn肥胖和胰岛素抵抗，短期的血浆胰岛素的变化并没有明显发挥调节作用外源性衍生的餐后脂蛋白。数据表明，胰岛素抵抗受试者的高乳糜微粒血症是胰岛素介导的餐后脂质代谢调节慢性失常的结果。
BackgroundObese, insulin‐resistant individuals have raised levels of intestinal and hepatic lipoproteins. Insulin decreases the production of hepatic lipoproteinsin vivo andso this study aimed to investigate whether an acute hyperinsulinaemic, euglycaemic clamp could correct fasting and post‐prandial dyslipidaemia.Subjects and methodsIn a randomized, cross‐over design, post‐prandial lipaemia was compared in subjects infused either with insulin to achieve a steady‐state concentration of 100 mU L−1or with saline. Nine obese (Body Mass Index > 26 kg m−2; waist : hip > 1·0) insulin‐resistant (Homeostatic Model Assessment score > 2·0) male subjects were given an oral fat load 3 h after the infusions began, and sampling continued for 6 h. Plasma apoB‐48, triglyceride and nonesterified fatty acid (NEFA) were measured hourly.ResultsAverage steady‐state serum insulin levels during the hyperinsulinaemic clamp were 123 ± 4·4 mU L−1. A paired analysis showed no net effect of insulin on post‐prandial chylomicron metabolism when calculated as the (apoB‐48) incremental area under the curve (IAUC). However, there was a trend towards a delay in the apoB‐48 peak, consistent with possible changes in the rates of chylomicron biogenesis, lipolysis and/or clearance. Similarly, post‐prandial lipaemia (depicted as triglyceride IAUC) was similar for subjects infused with insulin or saline, but the peak post‐prandial response was delayed during insulin infusion. The NEFA were rapidly decreased by 83% after 3 h of insulin infusion.ConclusionsIn obesity and insulin resistance, short‐term changes in plasma insulin do not appreciably exert a regulatory effect on exogenously‐derived post‐prandial lipoproteins. The data suggest that hyperchylomicronaemia in insulin‐resistant subjects is a result of chronic aberrations in insulin‐mediated regulation of post‐prandial lipid metabolism.