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目的探讨对初诊2型糖尿病患者行胰岛素强化治疗对海马N-乙酰天门冬氨酸复合物(NAA)/肌酸(Cr)、胆碱复合物(Cho)/肌酸(Cr)的长期影响。方法将58例初诊2型糖尿病患者随机分为2组,实验组29例予以早期胰岛素强化治疗,对照组29例予以常规口服降糖药物。于治疗前和1年后分别检测空腹血糖(FPG)、餐后2h血糖(2hPG)、糖化血红蛋白(HbAlc),并行胰岛素、C肽释放试验,计算C肽曲线下面积(AUCc-p)、HOMA-β细胞功能指数(HOMA-β)和HOMA-胰岛素抵抗指数(HOMA-IR),应用1 H-MRS检测左、右海马区NAA/Cr、Cho/Cr。结果治疗前实验组与对照组比较,FPG、2hPG、HbAlc,AUCc-p、HOMA-β、HOMA-IR,双侧海马NAA/Cr、Cho/Cr,差异均无统计学意义(P均>0.05)。治疗后1年实验组与对照组比较,FPG、2hPG、HbAlc差异均无统计学意义(P均>0.05);AUCc-p升高(P<0.05),HOMA-IR降低(P<0.05),HOMA-β差异无统计学意义(P>0.05);双侧海马NAA/Cr均升高(P均<0.05),Cho/Cr均降低(P均<0.05)。结论对2型糖尿病患者早期胰岛素强化治疗可影响海马NAA、Cho表达,并有一定的长期缓解作用,其机制可能与胰岛素抵抗改善有关。
Objective To investigate the long-term effects of insulin-enhanced therapy on NAA / Cr and Cr / Cr in newly diagnosed type 2 diabetic patients. Methods Fifty-eight newly diagnosed type 2 diabetic patients were randomly divided into two groups. 29 cases in the experimental group were treated with early intensive insulin therapy, and 29 cases in the control group were given routine oral antidiabetic drugs. Fasting blood glucose (FPG), postprandial 2h blood glucose (2hPG), HbAlc, parallel insulin and C peptide release test were measured before treatment and after 1 year to calculate the area under C-peptide curve (AUCc-p), HOMA β-cell function index (HOMA-β) and HOMA-insulin resistance index (HOMA-IR) were measured. Left and right hippocampus NAA / Cr and Cho / Cr were detected by 1H- Results There was no significant difference in FPG, 2hPG, HbAlc, AUCc-p, HOMA-β, HOMA-IR, NAA / Cr and Cho / Cr in bilateral hippocampus between the experimental group and the control group before treatment ). There was no significant difference in FPG, 2hPG and HbAlc between experimental group and control group at 1 year after treatment (P> 0.05), AUCc-p (P <0.05), HOMA-IR decreased There was no significant difference in HOMA-β between two groups (P> 0.05). NAA / Cr in bilateral hippocampus were both increased (P <0.05) and Cho / Cr decreased (all P <0.05). Conclusions Early insulin therapy in type 2 diabetic patients may affect the expression of NAA and Cho in hippocampus and have some long-term relief. The possible mechanism may be related to the improvement of insulin resistance.