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  • Author: Xinyi Zhao x
  • Metabolic Syndrome and Diabetes x
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Xue-Lian Zhang Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Xinyi Zhao Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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Yong Wu Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wen-qing Huang Department of Transfusion Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong, China

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Jun-jiang Chen Department of Physiology, School of Medicine, Jinan University, Guangzhou, China
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Peijie Hu Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Wei Liu Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Yi-Wen Chen Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Jin Hao Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Rong-Rong Xie Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Hsiao Chang Chan Epithelial Cell Biology Research Center, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China

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Ye Chun Ruan Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China

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Hui Chen Cell-Gene Therapy Translational Medicine Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China

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Jinghui Guo Department of Physiology, School of Medicine, Jinan University, Guangzhou, China

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Objective

The beneficial effect of angiotensin(1–7) (Ang(1–7)), via the activation of its receptor, MAS-1, has been noted in diabetes treatment; however, how Ang(1–7) or MAS-1 affects insulin secretion remains elusive and whether the endogenous level of Ang(1–7) or MAS-1 is altered in diabetic individuals remains unexplored. We recently identified an important role of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl channel, in the regulation of insulin secretion. Here, we tested the possible involvement of CFTR in mediating Ang(1–7)’s effect on insulin secretion and measured the level of Ang(1–7), MAS-1 as well as CFTR in the blood of individuals with or without type 2 diabetes.

Methods

Ang(1–7)/MAS-1/CFTR pathway was determined by specific inhibitors, gene manipulation, Western blotting as well as insulin ELISA in a pancreatic β-cell line, RINm5F. Human blood samples were collected from 333 individuals with (n  = 197) and without (n  = 136) type 2 diabetes. Ang(1–7), MAS-1 and CFTR levels in the human blood were determined by ELISA.

Results

In RINm5F cells, Ang(1–7) induced intracellular cAMP increase, cAMP-response element binding protein (CREB) activation, enhanced CFTR expression and potentiated glucose-stimulated insulin secretion, which were abolished by a selective CFTR inhibitor, RNAi-knockdown of CFTR, or inhibition of MAS-1. In human subjects, the blood levels of MAS-1 and CFTR, but not Ang(1–7), were significantly higher in individuals with type 2 diabetes as compared to those in non-diabetic healthy subjects. In addition, blood levels of MAS-1 and CFTR were in significant positive correlation in type-2 diabetic but not non-diabetic subjects.

Conclusion

These results suggested that MAS-1 and CFTR as key players in mediating Ang(1–7)-promoted insulin secretion in pancreatic β-cells; MAS-1 and CFTR are positively correlated and both upregulated in type 2 diabetes.

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