Evidence map›Paper›PMID 26648697›Full record

ArticleDrug design, development and therapy2015

Different effects of statins on induction of diabetes mellitus: an experimental study.

Wang Zhao, Shui-Ping Zhao

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% of its field
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Statin Use and Hyperglycemia: Do Statins Cause Diabetes?Current atherosclerosis reports · 2024
    Review
  8. Observational
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Statins Aggravate the Risk of Insulin Resistance in Human Muscle.International journal of molecular sciences · 2022
    Article
  18. Undertreatment or Overtreatment With Statins: Where Are We?Frontiers in cardiovascular medicine · 2022
    Review
  19. Review
  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

2 authors at 1 institution in 1 country.

Wang ZhaoDepartment of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Shui-Ping ZhaoDepartment of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo determine the effect of different statins on the induction of diabetes mellitus. MATERIALS AND

methodsFour statins (atorvastatin, pravastatin, rosuvastatin, and pitavastatin) were used. Cytotoxicity, insulin secretion, glucose-stimulated insulin secretion, and G0/G1 phase cell cycle arrest were investigated in human pancreas islet β cells, and glucose uptake and signaling were studied in human skeletal muscle cells (HSkMCs).

resultsHuman pancreas islet β cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had reduced cell viability (32.12%, 41.09%, 33.96%, and 29.19%, respectively) compared to controls. Such cytotoxic effect was significantly attenuated by decreasing the dose to 10 and 1 nM, ranged from 1.46% to 17.28%. Cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had a reduction in the rate of insulin secretion rate by 34.07%, 30.06%, 26.78%, and 19.22%, respectively. The inhibitory effect was slightly attenuated by decreasing the dose to 10 and 1 nM, ranging from 10.84% to 29.60%. Insulin secretion stimulated by a high concentration of glucose (28 mmol/L) was significantly higher than a physiologic concentration of glucose (5.6 mmol/L) in all treatment groups. The glucose uptake rates at a concentration of 100 nM were as follows: atorvastatin (58.76%) < pravastatin (60.21%) < rosuvastatin (72.54%) < pitavastatin (89.96%). We also found that atorvastatin and pravastatin decreased glucose transporter (GLUT)-2 expression and induced p-p38 MAPK levels in human pancreas islet β cells. Atorvastatin, pravastatin, and rosuvastatin inhibited GLUT-4, p-AKT, p-GSK-3β, and p-p38 MAPK levels in HSkMCs.

conclusionStatins similar but different degree of effects on pancreas islet β cells damage and induce insulin resistance in HSkMC.

Indexed as

AtorvastatinCell CycleCells, CulturedCell SurvivalDiabetes MellitusDose-Response Relationship, DrugGlucoseHumansInsulinInsulin ResistanceInsulin-Secreting CellsMuscle, SkeletalPravastatinQuinolinesRosuvastatin CalciumSignal TransductionAtorvastatinGlucoseInsulinpitavastatinPravastatinQuinolinesRosuvastatin Calciumglucosehuman pancreas islet β cellhuman skeletal muscle cellsinsulinstatins

Identifiers

PMID26648697
PMCPMC4664500
OpenAlexW2172799437

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.