EFFECTS OF A 48-H FAT INFUSION ON INSULIN-SECRETION AND GLUCOSE-UTILIZATION
EFFECTS OF A 48-H FAT INFUSION ON INSULIN-SECRETION AND GLUCOSE-UTILIZATION
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DOI：
10.2337/diabetes.44.10.1239
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发表时间：
1995-10-01
期刊：
影响因子：
7.7
通讯作者：
BARTON, M
中科院分区：
文献类型：
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作者：
BODEN, G;CHEN, XH;BARTON, M
为了确定血浆游离脂肪酸（FFA）长期升高对胰岛素分泌的影响，我们输注Liposyn II（4.3 μ mol . kg（-1）。min（-1））加肝素（0.4U. kg（-1）min（-1））静脉注射48 h。另外6名志愿者接受生理盐水输注，并作为对照受试者。在所有12名受试者（11名男性和1名女性）中，血糖被钳制在8.6 mmol/l。Liposyn/肝素输注导致血浆FFA浓度增加9.4倍（从132 μ mol/l到1，237 μ mol/l），胰岛素分泌率增加46%（241 ~ 352 pmol/min，P < 0.05）（通过血浆C-肽浓度的去卷积测定），并且在最初的24小时内下降30%，维持高血糖所需的葡萄糖输注速率（从55.5到39.1 μ mol kg（-1）min（-1），P < 0.02）。这种降低在第二个24小时内消失。总之，我们发现生理性升高的血浆FFA 1）增强葡萄糖刺激的胰岛素分泌48小时，2）最初引起外周胰岛素抵抗，其在第2天消失，可能是由于循环胰岛素水平升高。我们得出结论，在高血糖条件下的健康志愿者中，脂肪输注产生胰岛素抗性，其在类似于24小时后通过胰岛素的持续高分泌来补偿。
To determine the effects of prolonged elevation of plasma free fatty acids (FFAs) on insulin secretion, we infused Liposyn II (4.3 mu mol . kg(-1). min(-1)) plus heparin (0.4 U . kg(-1) min(-1)) intravenously into six healthy volunteers for 48 h. Another six volunteers received saline infusions and served as control subjects, In all 12 subjects (11 men and 1 woman), plasma glucose was clamped at similar to 8.6 mmol/l. Liposyn/heparin infusion resulted in a 9.4-fold increase in plasma FFA concentration (from 132 to 1,237 mu mol/l), a 46% increase in insulin secretion rates (from 241 to 352 pmol/min, P < 0.05) (determined by deconvolution of plasma C-peptide concentration), and a 30% decrease, during the initial 24 h, in the rate of glucose infusion needed to maintain hyperglycemia (from 55.5 to 39.1 mu mol kg(-1) min(-1), P < 0.02). This decrease disappeared during the second 24 h, In summary, we found that physiologically elevated plasma FFAs 1) potentiated glucose-stimulated insulin secretion for 48 h and 2) initially caused peripheral insulin resistance that disappeared during the 2nd day, probably as a result of elevated circulating insulin levels, We conclude that in healthy volunteers under hyperglycemic conditions, fat infusion produced insulin resistance that was compensated for after similar to 24 h by persistent hypersecretion of insulin.