血尿酸水平与糖尿病前期及2型糖尿病患者胰岛功能的相关分析

目的研究糖尿病前期及2型糖尿病（T2DM）患者的血尿酸(SUA)水平与胰岛功能的关系。方法纳入受试者4 112例，根据口服葡萄糖耐量试验(OGTT）将受试者分为3组：正常糖调节组（NGR）493例、糖调节受损组(IGR)1 251 例和T2DM组2 368例，分别测定3组SUA、空腹胰岛素(FIns)、餐后2 h胰岛素（2 h-Ins）水平，计算胰岛素抵抗指数（HOMA-IR），比较3组间SUA、胰岛素水平及HOMA-IR的差异；进一步对不同性别的SUA水平进行分层，比较各分层组间胰岛功能；通过双变量关联性分析IGR患者中SUA与胰岛功能异常的相关性。结果 IGR组SUA水平高于NGR及T2DM组（P<0.000 1），同时IGR组2 h-Ins水平高于NGR组及T2DM组（P<0.0001）；T2DM组FIns、HOMA-IR及糖化血红蛋白（HbA1c）水平高于NGR及IGR组（P<0.000 1）。对SUA水平分层分析发现，在男性不同SUA水平组，2 h-Ins水平在IGR组最高，而HOMA-IR及HbA1c在T2DM组最高。在女性不同SUA水平组，均是2 h-Ins水平在IGR组最高，而FIns、HOMA-IR及HbA1c在T2DM组最高。在男性和女性各SUA分组中，FIns及2 h-Ins随SUA水平的增高呈上升趋势。HOMA-IR在各SUA水平分组中，也随SUA增高呈上升趋势，且T2DM组最高。在相关性分析中，IGR组及T2DM组的FIns、2 h-Ins及HOMA-IR均与SUA有相关性，而HbA1c仅在T2DM组与SUA呈负相关。结论 SUA水平可能与糖尿病前期患者胰岛功能异常相关，因此SUA水平的检测对评估糖尿病前期患者进展为T2DM有潜在的应用价值。

英文摘要:

Objective To determine the correlation between serum uric acid (SUA) and insulin secretion function in patients with pre-diabetes and type-2 diabetes mellitus (T2DM). Methods A total of 4 112 adult people participated in this study. They were divided into three groups according to the results of oral glucose tolerance test (OGTT): 493 with normal glucose regulation (NGR), 1 251 with impaired glucose regulation (IGR), and 2 368 with T2DM. Their levels of SUA, fasting insulin (FIns), 2 h post-meal insulin (2 h-Ins), and insulin resistance index (HOMA-IR) were determined. Correlations between SUA and insulin secretion and HOMA-IR were estimated. Results IGR patients had higher levels of SUA and 2 h-Ins compared with those with NGR and T2DM (P<0.000 1). T2DM patients had higher levels of FIns, glucosylated hemoglobin (HbA1c） and HOMA-IR compared with those with NGR and IGR (P<0.000 1). In both male and female participants, the highest level of 2 h-Ins appeared in those with IGR, while T2DM had the highest level of HOMA-IA and HbA1c. FIns, 2 h-Ins and HOMA-IR increased with SUA in both patients with IGR and T2DM. HbA1c decreased with SUA in T2DM patients. Conclusion High serum SUA is correlated with islet β-cell dysfunction. It may become an indicator of progression from pre-diabetes to T2DM.

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