Hepatic production of VLDL1 but not VLDL2 is related to insulin resistance in normoglycaemic middle-aged subjects

Hepatic production of VLDL1 but not VLDL2 is related to insulin resistance in normoglycaemic middle-aged subjects
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DOI:
10.1016/j.atherosclerosis.2004.04.022
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发表时间:
2004-09-01
期刊:
影响因子:
5.3
通讯作者:
Caslake, MJ
Caslake, MJ
中科院分区:
医学2区
文献类型:
--
作者:
Gill, JMR;Brown, JC;Caslake, MJ

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胰岛素抵抗可能是代谢综合征的特征,也是血浆甘油三酯(TG)浓度的重要决定因素。我们试图调查胰岛素抵抗是否影响VLDL1(SF60-400)和VLDL2(SF20-60)的代谢。16名(8男,8女)血糖正常的中年受试者参与研究。用氚代亮氨酸示踪剂跟踪VLDL1和VLDL2载脂蛋白(Apo)B的代谢,并用稳态模型评估(HOMA)评估胰岛素抵抗。HOMA估计的胰岛素抵抗(HOMA(IR))与VLDL1产生率(r=0.69,P<0.01)和VLDL1载脂蛋白B池大小(r=0.59,P=0.02)显著相关,但对于VLDL2,这些关系不明显。反之,HOMAIR与VLDL1向VLDL2的转移率无显著相关,而与VLDL2向IDL的转移率显著相关(r=0.61,P=0.01)。HOMA(IR)与VLDL1或VLDL2的直接分解代谢分数无显著相关性。这些结果提示胰岛素抵抗在肝脏VLDL1生成中的决定作用,并突出了VLDL1和VLDL2代谢的独立调节。(C)2004爱思唯尔爱尔兰有限公司。保留所有权利。
Insulin resistance is probably the defining feature of the metabolic syndrome and is ail important determinant of plasma triglyceride (TG) concentrations. We sought to investigate whether insulin resistance influenced the metabolism of VLDL1 (Sf 60-400) and VLDL2 (Sf 20-60). Sixteen (eight men, eight women) middle-aged, normoglycaemic subjects participated. VLDL1 and VLDL2 apolipoprotein (apo) B metabolism was followed using a deuterated leucine tracer and insulin resistance was estimated using homeostasis model assessment (HOMA). HOMA-estimated insulin resistance (HOMA(IR)) significantly and strongly correlated with the VLDL1 production rate (r = 0.69, P < 0.01) and VLDL1 apo B pool size (r = 0.59, P = 0.02), but these relationships were not evident for VLDL2. Conversely, HOMAIR was not significantly related to the fractional rate of transfer of VLDL1 to VLDL2 but was significantly related to the fractional rate of transfer from VLDL2 to IDL (r = 0.61, P = 0.01). HOMA(IR) was not significantly related to the fractional rate of direct catabolism for either VLDL1 or VLDL2. These results suggest a role for insulin resistance in the determination of hepatic VLDL1 production and highlight the independent regulation of VLDL1 and VLDL2 metabolism. (C) 2004 Elsevier Ireland Ltd. All rights reserved.