Evidence map›Paper›PMID 25177911›Full record

ArticleNutrition & diabetes2014

Intermittent hypoxia-induced rat pancreatic β-cell apoptosis and protective effects of antioxidant intervention.

Y Fang, Q Zhang, J Tan, L Li, X An, P Lei

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrition & diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
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  11. Review
  12. Hypoxia Modulates Effects of Fatty Acids on NES2Y Human Pancreatic β-cells.International journal of molecular sciences · 2019
    Article
  13. Obstructive Sleep Apnea, Hypoxia, and Nonalcoholic Fatty Liver Disease.American journal of respiratory and critical care medicine · 2019
    Review
  14. Article
  15. Article
  16. [One-hour post-load plasma glucose: a better indicator of glucose metabolism for obstructive sleep apnea?]Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
  17. Review
  18. Review
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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.

Y FangTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.
Q ZhangTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.
J TanTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.
L LiTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.
X AnTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.
P LeiTianjin Medical University General Hospital, Department of Geriatrics, Tianjin Geriatrics Institute, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeObstructive sleep apnea hypopnea syndrome (OSAHS), a common sleep and breathing disorder, is independently associated with metabolic dysfunction, including impaired glucose tolerance and insulin resistance. Intermittent hypoxia (IH), a pathological component of OSAHS, increases oxidative stress damage to pancreatic β-cells in animal models resembling patients with OSAHS. However, the precise mechanisms of IH-induced pancreatic β-cell dysfunction are not fully understood. In the present study, we established a mice model to investigate the underlying mechanisms of oxidative stress in IH-induced pancreatic β-cell apoptosis through antioxidant N-acetylcysteine (NAC) pretreatment.

methodsTwenty-four Wistar rats were randomly divided into four experimental groups: normal control group, intermittent normoxia group, IH group and antioxidant intervention group. Pancreatic β-cell apoptosis rates were detected by terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling; Bcl-2 and Bax protein expressions were detected by immunohistochemistry staining and western blotting.

resultsIn our study, we demonstrated that IH exposure causes an increased activation of pancreatic β-cell apoptosis compared with that in the normal control group and intermittent normoxia group, accompanied by the downregulation of Bcl-2 and upregulation of Bax (P<0.05). Furthermore, compared with the IH group, antioxidant (NAC) pretreatment significantly decreased IH-mediated β-cell apoptosis and reversed the ratio of Bcl-2/Bax expression (P<0.05).

conclusionTaken together, these results demonstrate a critical role of oxidative stress in the regulation of apoptosis through Bcl-2 and Bax signaling. The antioxidant NAC has a protective effect against IH-induced pancreatic β-cell apoptosis.Nutrition & Diabetes advance online publication, __PUBDATE__; doi:10.1038/nutd.2014.28.

Identifiers

PMID25177911
PMCPMC4183969

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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.