EFFECTS OF ACUTE HYPERINSULINEMIA ON VLDL TRIGLYCERIDE AND VLDL APO-B PRODUCTION IN NORMAL-WEIGHT AND OBESE INDIVIDUALS
EFFECTS OF ACUTE HYPERINSULINEMIA ON VLDL TRIGLYCERIDE AND VLDL APO-B PRODUCTION IN NORMAL-WEIGHT AND OBESE INDIVIDUALS
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DOI：
10.2337/diabetes.42.6.833
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发表时间：
1993-06-01
期刊：
影响因子：
7.7
通讯作者：
STEINER, G
中科院分区：
文献类型：
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作者：
LEWIS, GF;UFFELMAN, KD;STEINER, G
短期高胰岛素血症对VLDL甘油三酯和VLDL apoB产生的影响在6小时正葡萄糖高胰岛素钳夹（40 MU. m-2 17名女性（8名慢性高胰岛素血症肥胖，BMI = 35.7 kg/m2; 9名正常体重，BMI = 22.5 kg/m2）。在急性高胰岛素血症期间，两组的血浆FFA在1小时内下降约95%。VLDL甘油三酯的产生在对照组中减少了66%（P = 0.0003），在肥胖组中减少了67%（P = 0.0003）。对照组ApoB的产生减少了53%（P = 0.03），而肥胖组仅减少了8%。对照组血浆甘油三酯较基线水平下降40%（P < 0.0001），但肥胖组仅下降10%（P = NS）。尽管在对照组中甘油三酯和apoB的产生类似的减少，但VLDL颗粒大小（甘油三酯与apoB的比率）随着高胰岛素血症而减少（P = 0.003）。在肥胖受试者中，尽管甘油三酯的产生与对照受试者相似，但载脂蛋白B的产生没有变化，VLDL的大小没有明显变化。人的急性高胰岛素血症1）在该高剂量的胰岛素下，在对照和肥胖受试者中同等地抑制血浆FFA; 2）在对照和肥胖受试者中同等地抑制VLDL甘油三酯产生，这可能继发于FFA的降低; 3）在对照中抑制VLDL apoB产生，但在肥胖受试者中抑制程度较低，这表明肥胖受试者可能对胰岛素的这种作用有抗性; 4）在对照受试者中降低血浆甘油三酯和VLDL颗粒尺寸，反映LPL活性的刺激或甘油三酯相对于apoB产生的更大相对降低;和5）在肥胖受试者中不降低血浆甘油三酯或VLDL尺寸至与在对照受试者中相同的程度。因此，肥胖的胰岛素抵抗影响VLDL代谢的一些方面，但不是所有方面。
The effects of short-term hyperinsulinemia on the production of both VLDL triglyceride and VLDL apoB were determined semiquantitatively before and during a 6-h euglycemic hyperinsulinemic clamp (40 MU. m-2 . min-1) in 17 women (8 chronically hyperinsulinemic obese, BMI = 35.7 kg/m2; 9 normal weight, BMI = 22.5 kg/m2). During acute hyperinsulinemia, plasma FFA decreased by approximately 95% within 1 h in both groups. VLDL triglyceride production decreased 66% in the control subjects (P = 0.0003) and 67% in obese subjects (P = 0.0003). ApoB production decreased 53% in control subjects (P = 0.03) but only 8% in obese (NS). Plasma triglycerides decreased by 40% from baseline in control subjects (P < 0.0001) but only by 10% in obese subjects (P = NS). Despite the similar decrease in triglyceride and apoB production in control subjects, VLDL particle size (triglyceride-to-apoB ratio) decreased with hyperinsulinemia (P = 0.003). In obese subjects, despite a decrease in triglyceride production similar to that in control subjects but no change in apoB production, VLDL size did not change appreciably. Acute hyperinsulinemia in humans 1) suppresses plasma FFA equally in control and obese subjects at this high dose of insulin; 2) inhibits VLDL triglyceride production equally in control and obese subjects, perhaps secondary to the decrease in FFA; 3) inhibits VLDL apoB production in control but less so in obese subjects, suggesting that obese subjects may be resistant to this effect of insulin; 4) decreases plasma triglyceride and VLDL particle size in control subjects, reflecting either stimulation of LPL activity or a greater relative decrease in triglyceride to apoB production; and 5) does not decrease plasma triglyceride or VLDL size in obese subjects to the same extent as it does in control subjects. Thus, the insulin resistance of obesity affects some but not all aspects of VLDL metabolism.