IGF-1 ameliorates streptozotocin-induced pancreatic β cell dysfunction and apoptosis via activating IRS1/PI3K/Akt/FOXO1 pathway

福克斯O1 蛋白激酶B PI3K/AKT/mTOR通路 内科学 胰岛素 内分泌学 活力测定 氧化应激 IRS1 胰岛素受体 细胞凋亡 化学 信号转导 生物 胰岛素抵抗 细胞生物学 医学 生物化学
作者
Fan Cui,Xin He
出处
期刊:Inflammation Research [Springer Science+Business Media]
卷期号:71 (5-6): 669-680 被引量:16
标识
DOI:10.1007/s00011-022-01557-3
摘要

Type 2 diabetes mellitus (T2DM) is an endocrine disorder with pancreatic β cell dysfunction and/or reduced insulin sensitivity. IGF-1 is critically involved in pancreatic β cell growth, differentiation, and insulin secretion. Insulin-mediated IRS1/PI3K/Akt/FOXO1 signaling has been proved to be closely associated with pancreatic β cell function, hepatic glucose metabolism, and the development of T2DM. This present work was designed to demonstrate the protective role of IGF-1 against pancreatic β cell dysfunction and to probe into the underlying mechanisms.Herein, cell viability, cell apoptosis, insulin secretion, oxidative stress, and glycolysis in STZ-treated INS-1 cells were measured, so as to determine the biological function of IGF-1 against pancreatic β cell dysfunction in T2DM. Additionally, whether IGF-1 could activate IRS1/PI3K/Akt/FOXO1 signaling pathway to manipulate the progression of T2DM was also investigated.It was discovered that IGF-1 treatment enhanced the viability and suppressed the apoptosis of STZ-treated INS-1 cells. Besides, IGF-1 treatment augmented insulin secretion of INS-1 cells in response to STZ. Moreover, IGF-1 exerted protective role against oxidative damage and displayed inhibitory effect on glycolysis in STZ-treated INS-1 cells. Mechanistically, IGF-1 treatment markedly boosted the activation of IRS1/PI3K/Akt/FOXO1 pathway. Furthermore, treatment with AG1024 (an inhibitor of IGF-1R) partially abolished the actions of IGF-1 on cell viability, cell apoptosis, insulin secretion, oxidative stress, and glycolysis in STZ-treated INS-1 cells.To conclude, IGF-1 could improve the viability and inhibit the apoptosis of STZ-treated pancreatic β cells, induce insulin secretion, alleviate oxidative damage, as well as arrest glycolysis by activating IRS1/PI3K/Akt/FOXO1 pathway.
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