Evidence map›Paper›PMID 25717351›Full record

ReviewWorld journal of biological chemistry2015

Chronic alcohol consumption potentiates the development of diabetes through pancreatic β-cell dysfunction.

Ji Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Jae Woo Kim, Won-Ho Kim

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Idiopathic chronic pancreatitis: clinical highlights.Therapeutic advances in gastroenterology · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Impact of binge drinking on alcoholic liver disease.Archives of pharmacal research · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 1 institution in 1 country.

Ji Yeon KimJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Dae Yeon LeeJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Yoo Jeong LeeJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Keon Jae ParkJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Kyu Hee KimJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Jae Woo KimJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Won-Ho KimJi Yeon Kim, Dae Yeon Lee, Yoo Jeong Lee, Keon Jae Park, Kyu Hee Kim, Won-Ho Kim, Division of Metabolic Diseases, Center for Biomedical Science, National Institute of Health, Osong-eup, Heungdeok-gu, Cheongju, Chungbuk 363-700, South Korea.
Korea National Institute of Health · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic ethanol consumption is well established as a major risk factor for type-2 diabetes (T2D), which is evidenced by impaired glucose metabolism and insulin resistance. However, the relationships between alcohol consumption and the development of T2D remain controversial. In particular, the direct effects of ethanol consumption on proliferation of pancreatic β-cell and the exact mechanisms associated with ethanol-mediated β-cell dysfunction and apoptosis remain elusive. Although alcoholism and alcohol consumption are prevalent and represent crucial public health problems worldwide, many people believe that low-to-moderate ethanol consumption may protect against T2D and cardiovascular diseases. However, the J- or U-shaped curves obtained from cross-sectional and large prospective studies have not fully explained the relationship between alcohol consumption and T2D. This review provides evidence for the harmful effects of chronic ethanol consumption on the progressive development of T2D, particularly with respect to pancreatic β-cell mass and function in association with insulin synthesis and secretion. This review also discusses a conceptual framework for how ethanol-produced peroxynitrite contributes to pancreatic β-cell dysfunction and metabolic syndrome.

Indexed as

Ethanol consumptionGlucokinaseMetabolic syndromePancreatic β-cellsType 2 diabetes

Identifiers

PMID25717351
PMCPMC4317634
OpenAlexW2312217825

What OpenQuestion holds

Textmetadata
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.