摘要
目的:探讨乙型肝炎(乙肝)后肝硬化患者糖代谢的临床特点及其发生机制。方法:选取乙肝后肝硬化患者35例作为肝硬化组,非肝病组44例作为对照,所有研究对象均行口服葡萄糖耐量试验(OGTT)联合胰岛素、C肽释放试验,测定其血糖(G)、胰岛素(INS)和C肽水平。结果:糖调节正常(NGR)或仅糖耐量异常(IGT)时,肝硬化组的胰岛素抵抗指数(HOMAIR)分别为5.72±2.15和4.98±2.70,胰岛素分泌指数(HOMAB)分别为105.88±37.86和67.53±24.99,均显著高于对照组的HOMAIR(1.62±0.34,2.72±1.62,P<0.05)和HOMAB(17.53±5.13,19.07±9.43,P<0.05);而其胰岛素指数(INSindex)分别为9.00±4.21和6.79±4.02显著低于对照组(23.46±11.59,17.24±7.52,P<0.05)。糖尿病(DM)时,肝硬化组与对照组间HOMAIR、HOMAB、INSindex值差别无统计学意义(P>0.05)。NGR或IGT时,C肽/INS比值(C/I)在肝硬化组与对照组间差别无统计学意义。DM时,C/I值在空腹及糖负荷后30min时两组间无显著差异,而在糖负荷后60、120、180min时肝硬化组的C/I值(分别为5.07±2.37、4.02±2.97和3.03±1.96)显著低于对照组(分别为8.60±2.95、8.31±2.92和11.89±4.22,P<0.05)。结论:乙肝后肝硬化患者在NGR或IGT时已存在胰岛素抵抗、空腹高胰岛素血症和糖负荷后的胰岛素早期分泌障碍;在DM时,由于肝损所致胰岛素在肝内代谢障碍,产生糖负荷后较低的C/I值,其为肝源性DM的特征性改变。因此,肝源性糖代谢异常的防治应从血糖正常时即开始,保护胰岛β细胞功能尤其重要。
Objective To explore the clinical characteristics and mechanism of glucose metabolism in patients with post-hepatitis B cirrhosis. Methods Thirty-five patients with post-hepatitis B cirrhosis and 44 patients without liver diseases as controls were gathered for oral glucose tolerance test （OGTT） in combination with insulin and C-peptide release test. The levels of plasma glucose, serum insulin and C-peptide were detected. Results In the subjects with normal glucose regulation （NGR） and impaired glucose tolerance （IGT）, HOMAIR were significantly higher in the cirrhosis group （5.72±2.15 and 4.98±2.70 respectively） than those in the control group （1.62±0.34 and 2.72±1.62 respectively, P〈0.05）; HOMAB were significantly higher in the cirrhosis group （105.88±37.86 and 67.53±24.99 respectively） than those in the control group （17.53±5.13 and 19.07±9.43 respectively, P〈0.05）, while the INSindex were significantly lower （9.00±4.21 and 6.79±4.02 respectively） than those in the control group （23.46±11.59 and 17.24±7.52 respectively, P〈0.05）. In the subjects with diabetes mellitus （DM）, no significant difference was discovered in HOMAIR, HOMAB and INSindex between the two groups. In the subjects with NGR and IGT, no significant difference was discovered in C-peptide/Insulin（C/I） between the two groups. In the subjects with DM, no significant difference was discovered for C/I between the two groups at fasting status and thirty minutes after glucose load. But at time of 60, 120 min after glucose load, there was significant difference between the cirrhosis group （5.07±2.37,4.02±2.97 and 3.03±1.96 respectively） and the control group （8.60±2.95,8.31±2.92 and 11.89±4.22 respectively, P〈0.05）. Conclusions In the patients with post-hepatitis B cirrhosis, there exists insulin resistance, hyper-insulinemia in fasting status and dysfunction in early-stage insulin secretion in states of NGR and IGT. When diabetes happens, insulin metabolism impairs due to liver dysfunction leading to lower ratio of plasma C-peptide and insulin after glucose load, which is the characteristic change in hepatogenous diabetes. Thus, the prevention of hepatogenous diabetes should start from the state of normal glucose regulation, especially the preservation of islet beta cell function.
出处
《诊断学理论与实践》
2007年第2期127-130,共4页
Journal of Diagnostics Concepts & Practice
