Evidence map›Paper›PMID 28598424›Full record

ArticleNature communications2017

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 1 more

Abstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed.

  1. Review
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  10. β-Cell Dedifferentiation in HOMA-βlow and HOMA-βhigh Subjects.The Journal of clinical endocrinology and metabolism · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Novel roles of mTORC2 in regulation of insulin secretion by actin filament remodeling.American journal of physiology. Endocrinology and metabolism · 2022
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Qicheng NiShanghai 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.ORCID 0000-0002-9033-9328
Yanyun GuShanghai 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 XieShanghai 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 YinShanghai 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 ZhangShanghai 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 NieShanghai 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 LiShanghai 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 WangShanghai 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 NingShanghai 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 WangShanghai 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 WangShanghai 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.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Cell DifferentiationAnimalsDiabetes Mellitus, Type 2DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3AFemaleGlucoseHumansInsulinInsulin-Secreting CellsMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutRegulatory-Associated Protein of mTORDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, humanDnmt3a protein, mouseGlucoseInsulinMechanistic Target of Rapamycin Complex 1Regulatory-Associated Protein of mTORRptor protein, mouse

Identifiers

PMID28598424
PMCPMC5472774

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.