GPCR信号依赖的六磷酸肌醇激酶1（IP6K1）磷酸化在胰岛素分泌中的作用探究

胰岛素是一种由胰岛β细胞分泌的多肽激素，对维持血糖浓度、调节机体葡萄糖稳态起重要作用。分泌至血液中的胰岛素量异常是糖尿病发病的根本原因。六磷酸肌醇（IP6）是一种在细胞中广泛存在、功能多样的高级磷酸肌醇，能被六磷酸肌醇激酶（IP6Ks）焦磷酸化生成焦磷酸肌醇（IP7）。已有研究表明，IP6K1与IP7能提高胰岛β细胞分泌能力，且IP6K1基因敲除小鼠中血清胰岛素含量显著低于野生型。这些结果均暗示IP6K1在体内可能具有调控胰岛素分泌的作用，但具体机制尚不明确。

Insulin, a peptide hormone synthesized and secreted by beta cells of the pancreatic islets, exerts its function in tightly regulating blood glucose concentration and thus reaching glucose homeostasis. One of the primary reasons for diabetes mellitus is the abnormal blood insulin levels. Inositol hexaphosphate (IP6) is an abundant endogenous metabolite that can be diphosphorylated by inositol hexaphosphate kinase (IP6Ks), generating inositol pyrophosphate (IP7). It is reported that IP6K1 and IP7 can promote the exocytotic ability of pancreatic beta cells. Besides, mice with IP6K1 deletion display low serum insulin levels. These results together indicate that IP6K1 play a role in regulating insulin homeostasis. However, the mechanism of which is still unclear.