Zheng Hai-Lan, Xing Yan, Li Fan, Ding Wei, Ye Shan-Dong
Shandong University School of Medicine, Jinan.
Department of Endocrinology, First People's Hospital of Anqing City, Anqing.
Medicine (Baltimore). 2020 Apr;99(14):e19685. doi: 10.1097/MD.0000000000019685.
The effect of intensive insulin therapy on hyperglucagonemia in newly diagnosed type 2 diabetes (T2DM), and its associations with β-cell function, has not been elucidated. This study assessed the effect of 12 weeks of intensive insulin therapy on hyperglucagonemia in newly diagnosed T2DM and its associations with β-cell function, with reference to the effects of 12 weeks of oral hypoglycemic agents (OHAs).One hundred eight patients with newly diagnosed T2DM were enrolled from January 2015 to December 2015. The patients were randomly divided to receive, for 12 weeks, either intensive insulin therapy or OHAs. Meal tolerance tests were conducted at baseline before treatment (0 week), at 12 weeks (end of treatment), and 12 months after the initiation of treatment. The levels of glucagon, proinsulin, C-peptide (CP), and blood glucose were measured at timepoints 0, 30, and 120 minutes during the meal tolerance test.Intensive insulin treatment was associated with a decrease in glucagon levels (at 0, 30, and 120 minutes) and proinsulin/CP, and an increase in the insulin-secretion index ΔCP30/ΔG30 and ΔCP120/ΔG120, at 12 weeks and 12 months during the follow-up, compared with the corresponding effects of OHAs. Intensive insulin therapy could reduce but failed to normalize glucagon levels at 12 weeks. There were no correlations between the change of percentages in total area under the curve of glucagon and other glycemic parameters (proinsulin/CP; ΔCP30/ΔG30; or ΔCP120/ΔG120). Patients who received intensive insulin therapy were more likely to achieve their target glycemic goal and remission, compared with those who received OHAs.Short-term intensive insulin therapy facilitates the improvement of both β-cell and α-cell function in newly diagnosed T2DM mellitus. Decline of β-cell secretion and concomitant α-cell dysfunction may both be involved in the pathogenesis of T2DM.
强化胰岛素治疗对新诊断2型糖尿病（T2DM）患者高胰高血糖素血症的影响及其与β细胞功能的关系尚未阐明。本研究评估了12周强化胰岛素治疗对新诊断T2DM患者高胰高血糖素血症的影响及其与β细胞功能的关系，并参考了12周口服降糖药（OHA）的效果。2015年1月至2015年12月纳入108例新诊断的T2DM患者。患者被随机分为两组，分别接受12周的强化胰岛素治疗或OHA治疗。在治疗前基线（0周）、12周（治疗结束时）和治疗开始后12个月进行进餐耐量试验。在进餐耐量试验的0、30和120分钟时间点测量胰高血糖素、胰岛素原、C肽（CP）和血糖水平。与OHA的相应效果相比，强化胰岛素治疗在随访的12周和12个月时与胰高血糖素水平（在0、30和120分钟时）和胰岛素原/CP的降低以及胰岛素分泌指数ΔCP30/ΔG30和ΔCP120/ΔG120的增加相关。强化胰岛素治疗在12周时可降低但未能使胰高血糖素水平恢复正常。胰高血糖素曲线下总面积百分比的变化与其他血糖参数（胰岛素原/CP；ΔCP30/ΔG30；或ΔCP120/ΔG120）之间无相关性。与接受OHA治疗的患者相比，接受强化胰岛素治疗的患者更有可能实现血糖目标并达到缓解。短期强化胰岛素治疗有助于改善新诊断T2DM患者的β细胞和α细胞功能。β细胞分泌减少和伴随的α细胞功能障碍可能均参与T2DM的发病机制。
