Comparisons between dipeptidyl peptidase-4 inhibitors and other classes of hypoglycemic drugs using two distinct biomarkers of pancreatic beta-cell function: A meta-analysis
Comparisons between dipeptidyl peptidase-4 inhibitors and other classes of hypoglycemic drugs using two distinct biomarkers of pancreatic beta-cell function: A meta-analysis
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DOI：
10.1371/journal.pone.0236603
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发表时间：
2020-07
期刊：
影响因子：
3.7
通讯作者：
Masahiro Takahashi;Misa Shibasaki;H. Echizen;A. Kushiyama
中科院分区：
文献类型：
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作者：
Masahiro Takahashi;Misa Shibasaki;H. Echizen;A. Kushiyama
背景与目的应用稳态β细胞功能评价模型（HOMA-β）研究表明，二肽基肽酶-4（DPP-4）抑制剂具有保护胰岛β细胞的作用。然而，HOMA-β是否是一个合适的生物标志物，用于比较具有不同作用机制的降糖药物仍不清楚。因此，我们进行了一项荟萃分析，以比较DPP-4抑制剂和其他类别的降糖药物对HOMA-β和胰岛素原/胰岛素比值（PIR）的影响。方法检索MEDLINE、CENTRAL和Ichushi-web，时间范围为1966年至2020年5月。我们收集了在2型糖尿病患者中比较DPP-4抑制剂与其他类别降糖药[α-葡萄糖苷酶抑制剂（α-GI）、胰高血糖素样肽-1（GLP-1）类似物、二甲双胍、钠-葡萄糖协同转运蛋白2（SGLT 2）抑制剂、磺脲类或噻唑烷二酮类]的随机对照临床试验。计算研究期间HOMA-β或PIR变化的加权平均差异和95%置信区间，以进行成对比较。结果分别检索到37篇和21篇相关文献进行HOMA-β和PIR的比较。HOMA-β和PIR一致显示DPP-4抑制剂优于α-GI。两种生物标志物一致支持DPP-4抑制剂劣于GLP-1类似物。然而，PIR显示DPP-4抑制剂劣效于二甲双胍，优效于SGLT 2抑制剂，而HOMA-β显示DPP-4抑制剂与其他两种药物之间无显著差异。结论DPP-4抑制剂在通过HOMA-β或PIR评估的β细胞功能保护方面似乎上级α-GI，但劣于GLP-1类似物。在仅通过PIR评估的胰岛功能方面，DPP-4抑制剂似乎上级于SGLT 2抑制剂，但劣于二甲双胍。由于HOMA-β和PIR可能指示β细胞功能的不同方面，因此应谨慎解释降糖药的β细胞功能保留作用的结果。
Background and objective Dipeptidyl peptidase-4 (DPP-4) inhibitors have been suggested to have pancreatic beta-cell preserving effect according to studies using homeostatic model of assessment for beta-cell function (HOMA-β). However, whether HOMA-β is a suitable biomarker for comparisons between hypoglycemic drugs with different mechanisms of action remains unclear. Therefore, we conducted a meta-analysis to compare the effects of DPP-4 inhibitors and other classes of hypoglycemic drugs on HOMA-β and proinsulin-to-insulin ratio (PIR). Methods We searched MEDLINE, CENTRAL, and Ichushi-web for the period of 1966 to May 2020. We collected randomized, controlled clinical trials in patients with type 2 diabetes mellitus comparing DPP-4 inhibitors and other classes of hypoglycemic agents [α-glucosidase inhibitors (α-GIs), glucagon-like peptide-1 (GLP-1) analogues, metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors, sulfonylureas, or thiazolidinediones]. Weighted mean differences and 95% confidence intervals of changes in HOMA-β or PIR during study periods were calculated for pairwise comparisons. Results Thirty-seven and 21 relevant trials were retrieved for comparisons of HOMA-β and PIR, respectively. HOMA-β and PIR consistently showed superiority of DPP-4 inhibitors compared with α-GIs. Both biomarkers consistently supported inferiority of DPP-4 inhibitors compared with GLP-1 analogues. However, PIR showed inferiority of DPP-4 inhibitors compared with metformin, and superiority compared with SGLT2 inhibitors, whereas HOMA-β showed no significant differences between DPP-4 inhibitors and the two other agents. Conclusion DPP-4 inhibitors appear to be superior to α-GIs but inferior to GLP-1 analogues in preservation of beta-cell function assessed by either HOMA-β or PIR. DPP-4 inhibitors seem to be superior to SGLT2 inhibitors but inferior to metformin on islet function assessed only by PIR. Because HOMA-β and PIR may indicate different aspects of beta-cell function, results of beta-cell function preserving effects of hypoglycemic agents should be interpreted with caution.