肥胖病高胰岛素血症发生机制的探讨

The Pathogenesis of Hyperinsulinemia in Obesity

采用放射免疫和放射受体测定法,对30例肥胖病患者及15名健康受试者(NWNT)血清中免疫反应性胰岛素(IRI)、免疫反应性C肽(IRCP)和红细胞胰岛素受体进行测定。结果显示:(1)肥胖病糖耐量降低的患者(OIT)和肥胖病伴有糖耐量严重降低的Ⅱ型糖尿病患者(OD)血清IRI水平和C肽水平较NWNT组明显升高(P<0.01和P<0.05),而糖耐量正常的肥胖病患者(ONT)与NWNT组间比较无显著性差异。(2)IRCP/IRI摩尔比值在OIT和OD组比NWNT组明显下降(P<0.05和P<0.01)。(3)OIT和OD组红细胞胰岛素受体数目明显降低(均P<0.05),而受体亲和力无明显改变。结果提示:肥胖病的高胰岛素血症机制可能是β细胞分泌、胰岛素清除和胰岛素受体结合障碍造成的。

The levels of serum glucose(SG), immunoreactive insulin(IRI) , immunoreactive C peptide( IRCP), and insulin binding to its receptor were determined by the methods of RIA and RRA in 30 obese patients and 15 normal subjects. The results showed: (1)The fasting insulin and C-peptide levels were significantly higher in obese either with glucose intolerance(OIT) ,or with Ⅱ type diabetes(OD) than in normotol-erant normal-weight control(NWNT)(P<0.01 and P<0.05), whereas no significant differences between NWNT and normotolerant obese patients(ONT). (2)The C-peptide/insulin(IRCP/IRI)molar ratio in OIT and OD groups were lower than in NWNT groups,and (3) Scatchard plot analysis of insulin binding to erythrocvtes from OIT and OD showed a reduced number of receptors(P<0.05) .whereas no significant differences in receptor affinity compared to NWNT. All above suggests:The pathogenetic mechanism of hyperinsulinemia in obese patients with impaired glucose tolerance was mainly due to the disorders of pancreatic β cell secretion,insulin clearance,and insulin binding to its receptor.