The loss of beta-cell functional mass is a necessary and early condition in the development of type 2 diabetes (T2D). In T2D patients, beta-cell function is already reduced by about 50% at diagnosis and further declines thereafter. Beta-cell mass is also reduced in subjects with T2D, and islets from diabetic donors are smaller compared to non-diabetic donors. Thus, beta-cell regeneration and/or preservation of the functional islet integrity should be highly considered for T2D treatment and possibly cure. To date, the available anti-diabetes drugs have been developed as “symptomatic” medications since they act to primarily reduce elevated blood glucose levels. However, a truly efficient anti-diabetes medication, capable to prevent the onset and progression of T2D, should stop beta-cell loss and/or promote the restoration of fully functional beta-cell mass, independently of reducing hyperglycemia and ameliorating glucotoxicity on the pancreatic islets. This review provides a view of the experimental and clinical evidence on the ability of available anti-diabetes drugs to exert protective effects on beta-cells, with a specific focus on human pancreatic islets and clinical trials. Potential explanations for the lack of concordance between evidence of beta-cell protection in vitro and of persistent amelioration of beta-cell function in vivo are also discussed.

在2型糖尿病（T2D）的发展中，β细胞功能的丧失是必要的早期条件。在T2D患者中，诊断时β细胞功能已经降低了约50％，此后进一步下降。在患有T2D的受试者中，β细胞的质量也降低了，与非糖尿病供体相比，糖尿病供体的胰岛更小。因此，对于T2D治疗和可能的治愈，应高度考虑β细胞的再生和/或功能性胰岛完整性的保存。迄今为止，可用的抗糖尿病药已被开发为“有症状的”药物，因为它们主要起降低血糖水平的作用。但是，真正有效的抗糖尿病药物能够预防T2D的发作和发展，应当独立于降低高血糖症和改善胰岛的糖毒性而停止β细胞的丢失和/或促进功能完整的β细胞的恢复。这篇综述提供了有关可用的抗糖尿病药物对β细胞发挥保护作用的能力的实验和临床证据的观点，特别是针对人胰岛和临床试验。关于β细胞保护证据之间缺乏一致性的潜在解释还讨论了体外和体内β细胞功能的持续改善。