3c型糖尿病（T3cDM），又称胰源性糖尿病，是由慢性胰腺炎等胰腺外分泌组织损伤引发胰岛内分泌功能紊乱而发生，其患病率约占糖尿病的5～10%。在T3cDM发生过程中，慢性炎症损伤胰岛β细胞，胰岛素分泌减少致血糖升高；同时，外分泌腺泡细胞还分泌大量胰腺再生蛋白（Reg1），被认为是胰岛β细胞再生因子。然而，Reg1是如何穿越破坏的胰腺内、外分泌屏障进入胰岛内对β细胞进行调控尚不清楚。我们前期研究发现，在胰腺损伤中Reg1可抑制胰腺星状细胞活性，逆转胰腺纤维化并促进组织再生修复，这可能是胰腺受损后的一种自我保护机制。但Reg1在T3cDM发生过程中对胰岛β细胞的作用尚未阐明。本研究拟在已成功建立的T3cDM小鼠模型基础上，探索胰腺内、外分泌之间的相互联系，探讨Reg1对β细胞的保护和促进再生作用及机制，以期对T3cDM发展过程有全新的认识，为防治T3cDM提供新思路。

Type 3c diabetes mellitus (T3cDM), also known as pancreatogenic diabetes, is a type of diabetes caused by the damage of pancreatic exocrine tissues such as chronic pancreatitis, which affects the endocrine function of islets. The prevalence of T3cDM is about 5-10%. During the development of T3cDM, chronic inflammation damages pancreatic beta cells, and insulin secretion decreases, resulting in increased blood sugar. At the same time, exocrine acinar cells also secrete a large amount of pancreatic regeneration protein (Reg1), which is recognized as islet beta cell regeneration factor. However, how Reg1 crosses the damaged pancreatic endocrine and exocrine barriers and enters the islets to regulate beta cells remains unclear. We have done a series studies on the function of Reg1 in pancreatic injury. We found that Reg1 can inhibit the activation of pancreatic stellate cells, reverse pancreatic fibrosis and promote tissue regeneration and repair, which may be a self-protective mechanism after pancreatic injury. However, the effect of Reg1 on islet beta cells in the development of T3cDM has not been elucidated. This study aims to explore the relationship between endocrine and exocrine secretions of pancreas and the protective and regenerative effects of Reg1 on beta cells on the basis of our established T3cDM mice model, so as to have a new understanding of the development of T3cDM and provide new ideas for the prevention and treatment of T3cDM.