SIRT1 Activation Promotes β-Cell Regeneration by Activating Endocrine Progenitor Cells via AMPK Signaling-Mediated Fatty Acid Oxidation

被引:24
作者
Wu, Shang Ying [1 ]
Liang, Juan [1 ]
Yang, Bao Chen [1 ]
Leung, Po Sing [1 ,2 ]
机构
[1] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Room 609A, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Key Lab Regenerat Med,Minist Educ, Hong Kong, Peoples R China
关键词
Diabetes; SIRT1; beta-Cell regeneration; Endocrine progenitors; NGN3; Pancreatic ductal cells; Pancreas development; Metabolism; II TYPE-2 RECEPTOR; CALORIE RESTRICTION; DIFFERENTIATION; MECHANISMS; PANCREAS; NEUROGENIN3; METABOLISM; MTORC1;
D O I
10.1002/stem.3073
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Induction of beta-cell regeneration from endogenous cells represents a highly promising strategy in stem cell-based treatment for patients with diabetes. Recently, calorie restriction has been shown to affect the regulation of tissue and cell regeneration, including beta cells, via metabolic related mechanisms. Here, we examined the potential utility of sirtuin 1 (SIRT1), a calorie restriction mimetic, for stimulating beta-cell regeneration and the underlying mechanisms of such stimulation. The present results showed that SIRT1 activation with SRT1720 promoted beta-cell regeneration in streptozotocin (STZ)-induced beta-cell-deficient neonatal rats. This beneficial effect involved enhanced activation of neurogenin3 (NGN3)-positive endocrine progenitors from pancreatic ductal cells, rather than an expansion of residual beta cells. A dynamic expression profile of SIRT1 was observed in endocrine progenitors both during beta-cell regeneration in neonatal rats and in the second transition phase of mouse pancreas development. Consistently, SRT1720 treatment upregulated endocrine progenitor differentiation in cultured pancreatic rudiments. Upregulation of NGN3 by SIRT1 activation was through stimulating AMP-activated protein kinase (AMPK) signaling-mediated fatty acid oxidation (FAO) in human pancreatic progenitor cells; AMPK inhibition abolished these effects. The present findings demonstrate a promotional effect of SIRT1 activation on beta-cell restoration and endocrine progenitor differentiation that involves regulation of AMPK signaling-mediated FAO. Stem Cells 2019
引用
收藏
页码:1416 / 1428
页数:13
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