PERIPHERAL HYPERINSULINEMIA OF SIMPLE OBESITY - PANCREATIC HYPERSECRETION OR IMPAIRED INSULIN METABOLISM
PERIPHERAL HYPERINSULINEMIA OF SIMPLE OBESITY - PANCREATIC HYPERSECRETION OR IMPAIRED INSULIN METABOLISM
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DOI：
10.1210/jcem-59-6-1121
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发表时间：
1984-01-01
影响因子：
5.8
通讯作者：
BUTTURINI, U
中科院分区：
文献类型：
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作者：
BONORA, E;ZAVARONI, I;BUTTURINI, U
测量了65名非糖尿病肥胖受试者、65名年龄和性别匹配的非糖尿病肥胖受试者和65名年龄和性别匹配的正常体重的非糖尿病受试者的空腹和口服葡萄糖负荷后外周血中的胰岛素和c肽水平。肥胖受试者的空腹胰岛素和c肽水平明显高于非肥胖受试者，而在口服葡萄糖负荷后1和2小时，肥胖受试者只有胰岛素浓度显著高于非肥胖受试者。用c肽与胰岛素的摩尔比以及两种肽增量面积的关系作为肝胰岛素提取的相对指标。在空腹状态下，肥胖者和非肥胖者的c肽和胰岛素的比值相似，而在摄入葡萄糖后，肥胖者的c肽和胰岛素的比值明显降低。同样，c肽与胰岛素增量区域之间的关系在肥胖受试者中明显低于非肥胖受试者。葡萄糖后c肽与胰岛素对应的血浆水平及面积的比较表明，对于相同的c肽值，肥胖组的胰岛素值更高。最后，在肥胖受试者中，用于估计口服葡萄糖后肝脏胰岛素去除的参数与空腹胰岛素浓度和葡萄糖后胰岛素增量面积呈负相关。在肥胖中，外周高胰岛素血症显然取决于空腹状态下胰腺胰岛素的高分泌和口服葡萄糖负荷后肝脏胰岛素代谢受损。
Insulin and C-peptide levels in peripheral blood in the fasting state and after an oral glucose load were measured in 65 nondiabetic, obese subjects and 65 age- and sex-matched nondiabetic, obese subjects nad 65 age- and sex-matched nondiabetic normal weight subjects. Fasting insulin and C-peptide levels were significantly higher in obese than in nonobese subjects, whereas 1 and 2 h after the oral glucose load only insulin concentrations were significantly higher in the obese subjects. C-peptide to insulin molar ratios, as well as the relation between the incremental areas of the 2 peptides, were used as relative measures of hepatic insulin extraction. In the fasting state the ratios between C-peptide and insulin were similar in obese and nonobese subjects, whereas after glucose they were significantly lower in the obese individuals. Similarly, the relations between C-peptide and insulin incremental areas were significantly lower in obese than in nonobese subjects. The comparison of the corresponding plasma levels and areas of C-peptide and insulin after glucose showed that for the same C-peptide value, the insulin value was higher in the obese group. Last, in obese subjects the parameter used as an estimate of hepatic removal of insulin after oral glucose inversely correlated with the fasting insulin concentration and the insulin incremental area after glucose. In obesity, peripheral hyperinsulinemia apparently depends on pancreatic hypersecretion of insulin in the fasting state and impaired hepatic insulin metabolism after oral glucose loading.