非酒精性脂肪性肝病进展性肝纤维化患者空腹血糖受损和胰岛素抵抗调查*

目的 调查非酒精性脂肪性肝病(NAFLD)患者空腹血糖受损(IFG)和胰岛素抵抗情况及其与肝纤维化的关系。方法 2020年5月～2021年5月我院健康管理门诊诊治的NAFLD患者110例,接受口服葡萄糖耐量试验(OGTT)试验。计算稳态模型胰岛素抵抗指数(HOMA-IR),采用放射免疫法测定血清Ⅳ型胶原、Ⅲ型前胶原(PCⅢ)、层黏连蛋白(LN)和透明质酸(HA)。计算NAFLD纤维化评分(NFS),以NFS﹥0.676被定义为存在进展性肝纤维化。应用Logistic回归模型分析影响NAFLD患者发生进展性肝纤维化的因素。结果 经OGTT试验,发现本组糖耐量正常(NGT)者43例,糖耐量异常(IGT)者35例和IFG者32例;IFG组空腹血糖(FPG)、胰岛素(FINS)和HOMA-IR指数分别为(6.6±0.3)mmol/L、(10.9±2.4)μU/mL和3.2±0.9,显著高于IGT组【分别为(5.6±0.7)mmol/L、(8.5±2.2)μU/mL和2.4±0.5,P＜0.05】或NGT组【分别为(5.5±0.6)mmol/L、(7.4±1.9)μU/mL和1.8±0.4,P＜0.05】,而IGT组FINS和HOMA-IR指数显著高于NGT组(P＜0.05);IFG组血清Ⅳ型胶原、PCⅢ、LN和HA水平分别为(75.7±9.6)ng/mL、(146.3±13.1)ng/mL、(132.7±15.2)ng/mL和(189.6±17.5)ng/mL,显著高于IGT组【分别为(63.9±8.4)ng/mL、(133.3±10.7)ng/mL、(122.4±13.4)ng/mL和(163.9±18.6)ng/mL,P＜0.05】或NGT组【分别为(59.4±7.4)ng/mL、(128.6±11.6)ng/mL、(109.4±8.9)ng/mL和(150.2±13.2)ng/mL,P＜0.05】,而IGT组Ⅳ型胶原、LN和HA水平显著高于NGT组(P＜0.05);本组18例患者被判断为存在进展性肝纤维化。多因素Logistic回归分析结果显示,IFG(OR=1.528)和IR(OR=1.714)是NAFLD患者发生进展性肝纤维化的独立危险因素(P＜0.05)。结论 NAFLD患者发生IFG时已存在明显的胰岛素抵抗,可能促进了肝纤维化进程。

Impact of impaired fasting glucose and insulin resistance on liver fibrosis in patients with nonalcoholic fatty liver diseases

Objective The aim of this study was to analyze the impact of impaired fasting glucose (IFG) and insulin resistance (IR) on liver fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Methods A total of 110 patients with NAFLD were encountered in the Health Management Clinic between May 2020 and May 2021. All individuals underwent oral glucose tolerance test (OGTT), and the homeostasis model insulin resistance index (HOMA-IR) was calculated. Serum type IV collagen, type III procollagen (PCIII), laminin (LN) and hyaluronic acid (HA) levels were detected by radioimmunoassay. The NAFLD fibrosis score (NFS) was calculated and the progressive liver fibrosis (PLF) was defined as the NFS﹥0.676. The multivariate Logistic regression analysis was applied to reveal the risk factors for PLF occurrence. Results Based on the OGTT results, the normal glucose tolerance (NGT) was found in 43 cases, the impaired glucose tolerance (IGT) in 35 cases and the IFG in 32 cases; the fasting plasma glucose, insulin and HOMA-IR in patients with IFG were (6.6±0.3) mmol/L, (10.9±2.4) μU/mL and 3.2±0.9, significantly higher than (5.6±0.7) mmol/L, (8.5±2.2) μU/mL and 2.4±0.5, P<0.05] in patients with IGT or (5.5±0.6) mmol/L, (7.4±1.9) μU/mL and 1.8±0.4, P<0.05] in patients with NGT; serum collagen IV, PCIII, LN and HA levels in patients with IFG were (75.7±9.6) ng/mL, (146.3±13.1) ng/mL, (132.7±15.2) ng/mL and (189.6±17.5) ng/mL, significantly higher than (63.9 ± 8.4) ng/mL, (133.3 ± 10.7) ng/mL, (122.4 ± 13.4) ng/mL and (163.9 ± 18.6) ng/mL, P<0.05] in patients with IGT or (59.4 ± 7.4) ng/mL, (128.6 ± 11.6) ng/mL, (109.4 ± 8.9) ng/mL and (150.2 ± 13.2) ng/mL, P<0.05] in patients with NGT; the PLF was found in 18 patients in our series, and the multivariate Logistic regression analysis showed that the IFG (OR=1.528) and IR (OR=1.714) were the independent risk factors for PLF in patients with NAFLD (P<0.05). Conclusion When the IFG occurs in patients with NAFLD hint the IR, which might promote liver fibrosis progression.