Shumak S L, Zinman B, Zuniga-Guarjardo S, Poapst M, Steiner G
Division of Endocrinology and Metabolism, Toronto General Hospital, Ontario, Canada.
Metabolism. 1988 May;37(5):461-6. doi: 10.1016/0026-0495(88)90047-9.
Chronic endogenous hyperinsulinemia is associated with increased rates of triglyceride production in humans. The effect of acute exogenous hyperinsulinemia on triglyceride production was studied in seven hypertriglyceridemic men before and during six hours of hyperinsulinemic-euglycemic clamping, and in two men before and during six hours of hyperinsulinemic-hyperglycemic clamping. Apparent triglyceride production rates were assessed qualitatively by examining the rate of decline of 3H-glycerol-labeled plasma triglyceride specific activity in the preclamp period, and again when a new steady state had occurred, during the final three hours of the clamp. During the euglycemic (91.2 +/- 3.0 mg glucose/dL plasma) clamps, plasma insulin levels were increased by 700% (0.76 +/- 0.12 to 5.3 +/- 0.29 ng/mL, P less than .001) and plasma glucagon levels decreased by 19%, compared with baseline. The apparent triglyceride production rate did not increase in five of six men during the euglycemic-hyperinsulinemic clamp, or in either man during the hyperglycemic-hyperinsulinemic clamp. During the clamp period the triglyceride declined in the plasma by 23.4 +/- 3.1%; and the apolipoprotein B by 10.5 +/- 1.5%. Hyperinsulinemia with euglycemia was also associated with a decline in the ratio of triglyceride to apolipoprotein B in the triglyceride-rich lipoproteins. This was more pronounced in very low density lipoprotein (VLDL) than in intermediate density lipoprotein (IDL). In this study, hyperinsulinemia led to a decrease in the plasma glucagon concentration. This decrease was positively correlated with the decrease in the slope of the triglyceride specific activity v time curve. Hence, the changes in triglyceride production were not due to an increase in plasma glucagon concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
慢性内源性高胰岛素血症与人类甘油三酯生成率增加有关。在7名高甘油三酯血症男性进行6小时高胰岛素-正常血糖钳夹的前后，以及2名男性进行6小时高胰岛素-高血糖钳夹的前后，研究了急性外源性高胰岛素血症对甘油三酯生成的影响。通过在钳夹前阶段以及在钳夹最后三小时出现新的稳定状态时，检查3H-甘油标记的血浆甘油三酯比活性的下降速率，定性评估表观甘油三酯生成率。在正常血糖（血浆葡萄糖91.2±3.0mg/dL）钳夹期间，与基线相比，血浆胰岛素水平增加了700%（从0.76±0.12ng/mL增至5.3±0.29ng/mL，P<0.001），血浆胰高血糖素水平下降了19%。在6名男性中的5名进行正常血糖-高胰岛素钳夹期间，以及在2名男性进行高血糖-高胰岛素钳夹期间，表观甘油三酯生成率均未增加。在钳夹期间，血浆中甘油三酯下降了23.4±3.1%；载脂蛋白B下降了10.5±1.5%。正常血糖伴高胰岛素血症还与富含甘油三酯脂蛋白中甘油三酯与载脂蛋白B的比率下降有关。这在极低密度脂蛋白（VLDL）中比在中间密度脂蛋白（IDL）中更明显。在本研究中，高胰岛素血症导致血浆胰高血糖素浓度降低。这种降低与甘油三酯比活性对时间曲线斜率的降低呈正相关。因此，甘油三酯生成的变化并非由于血浆胰高血糖素浓度增加所致。（摘要截短至250字）
