Raptor regulates functional maturation of murine beta cells

Qicheng Ni, Yanyun Gu, Yun Xie, Qinglei Yin, Hongli Zhang, Aifang Nie, Wenyi Li, Yanqiu Wang, Guang Ning, Weiqing Wang () and Qidi Wang ()
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Qicheng Ni: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Yanyun Gu: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Yun Xie: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Qinglei Yin: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Hongli Zhang: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Aifang Nie: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Wenyi Li: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Yanqiu Wang: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Guang Ning: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Weiqing Wang: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China
Qidi Wang: Shanghai National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of Chinese Health Ministry, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, 200025 Shanghai, China

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Diabetes is associated with beta cell mass loss and islet dysfunctions. mTORC1 regulates beta cell survival, proliferation and function in physiological and pathological conditions, such as pregnancy and pancreatectomy. Here we show that deletion of Raptor, which is an essential component of mTORC1, in insulin-expressing cells promotes hypoinsulinemia and glucose intolerance. Raptor-deficient beta cells display reduced glucose responsiveness and exhibit a glucose metabolic profile resembling fetal beta cells. Knockout islets have decreased expression of key factors of functional maturation and upregulation of neonatal markers and beta cell disallowed genes, resulting in loss of functional maturity. Mechanistically, Raptor-deficient beta cells show reduced expression of DNA-methyltransferase 3a and altered patterns of DNA methylation at loci that are involved in the repression of disallowed genes. The present findings highlight a novel role of mTORC1 as a core mechanism governing postnatal beta cell maturation and physiologic beta cell mass during adulthood.

Date: 2017
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DOI: 10.1038/ncomms15755

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