Evidence map›Paper›PMID 25367288›Full record

ArticleScientific reports2014

Arsenic induces diabetic effects through beta-cell dysfunction and increased gluconeogenesis in mice.

Su Liu, Xuechao Guo, Bing Wu, Haiyan Yu, Xuxiang Zhang, Mei Li

Abstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Type 2 diabetes mellitus and zinc dysregulation: From basic and epidemiological evidence to interventions.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
    Review
  6. Article
  7. Article
  8. Metabolic Derangement by Arsenic: a Review of the Mechanisms.Biological trace element research · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors.

Su LiuState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.
Xuechao GuoState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.
Bing WuState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.
Haiyan YuState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.
Xuxiang ZhangState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.
Mei LiState key laboratory of Pollution control and resource reuse, School of the Environment, Nanjing University, Nanjing, 210023, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic as a potential risk factor for type 2 diabetes has been received attention recently. However, the roles of arsenic on development of diabetes are unclear. In this study, we compared the influences of inorganic arsenic (iAs) on normal and diabetic mice by systems toxicology approaches. Although iAs exposure did not change glucose tolerance in normal mice, it caused the pancreatic β-cell dysfunction and increased gluconeogenesis and oxidative damages in liver. However, iAs exposure worsened the glucose tolerance in diabetic mice, which might be due to increased gluconeogenesis and impairment of pancreatic β-cell function. It is interesting that iAs exposure could improve the insulin sensitivity based on the insulin tolerance testing by the activation of glucose uptake-related genes and enzymes in normal and diabetic individuals. Our data suggested that iAs exposure could cause pre-diabetic effects by altering the lipid metabolism, gluconeogenesis and insulin secretion in normal individual, and worsen diabetic effects in diabetes individual by these processes. Insulin resistance might be not the reason of diabetic effects caused by iAs, indicating that mechanism of the diabetogenic effects of iAs exposure is different from the mechanism associated with traditional risk factors (such as obesity)-reduced type 2 diabetes.

Indexed as

AnimalsArsenicDiabetes Mellitus, Type 2Energy IntakeGluconeogenesisGlucose IntoleranceInflammationInsulin ResistanceInsulin-Secreting CellsLipid MetabolismMaleMice, Inbred C57BLOxidative StressPancreasWater Pollutants, ChemicalArsenicWater Pollutants, Chemical

Identifiers

PMID25367288
PMCPMC4219158

What OpenQuestion holds

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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.