论文部分内容阅读
目的 :探讨慢肝患者糖代谢异常的发病机理。方法 :对 35例慢性肝病患者进行糖耐量试验 ,同步应用放免法检测 IRI、C肽、K1 - 2 、R1 - 2 ;计算 ISI并与年龄、K1 - 2 、R1 - 2 以及各时相 IRI、C肽进行多元相关分析。结果 :慢肝特别是肝硬化病人呈现进行性血糖升高。当发展到糖耐量损害时 ,血糖高峰移行至餐后 1～ 3h,伴随餐后 2～ 3h高 IRI、 C肽血症、R1 - 2 下降、胰岛素敏感指数减低并与 IRI、C肽呈负相关 ,与年龄、K1 、R2 呈正相关。结论 :慢肝患者糖耐量损害是肝脏以及靶组织受体和受体后胰岛素抵抗等综合因素相互作用的结果。
Objective: To investigate the pathogenesis of abnormal glucose metabolism in patients with chronic liver disease. Methods: The glucose tolerance test was performed in 35 patients with chronic liver disease. The IRI, C - peptide, K1 - 2 and R1 - 2 were simultaneously detected by radioimmunoassay. The ISI was calculated and correlated with age, K1 - C peptide for multivariate correlation analysis. Results: Progressive hyperglycemia was found in patients with chronic liver disease, especially cirrhosis of the liver. When the development of impaired glucose tolerance, the peak of blood glucose shifted to 1 ~ 3h postprandial, accompanied by high IRI and C - peptide hyperlipidemia after 2 ~ 3hours postprandial, the decrease of R1 - 2 and the decrease of insulin sensitivity index and negatively correlated with IRI and C peptide , And age, K1, R2 was positively correlated. Conclusion: The impaired glucose tolerance in patients with chronic liver disease is the result of the interaction between liver and target tissue receptors and post-receptor insulin resistance.