Evidence map›Paper›PMID 19933995›Full record

ArticleDiabetes2010

Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the pancreatic beta-cells and islets enhance insulin secretion and confer protection against cytokine-induced cell death.

Dong Wei, Jie Li, Miaoda Shen, Wei Jia, Nuoqi Chen, Tao Chen, Dongming Su, Haoming Tian, Shusen Zheng, Yifan Dai and 1 more

Abstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
5.9field-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

65 citing papers in PubMed, 133 citations in OpenAlex.

  1. Trial
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  3. Review
  4. GαJournal of the Endocrine Society · 2024
    Article
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  8. Article
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  15. Article
  16. The Effect of Omega-3 Fatty Acids on Rheumatoid Arthritis.Mediterranean journal of rheumatology · 2020
    Review
  17. Frontiers in microbiology · 2020
    Review
  18. Article
  19. Review
  20. Article

5 more citing papers are in PubMed but not listed here.

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 at 5 institutions in 2 countries.

Dong WeiDepartment of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Jie Li
Miaoda Shen
Wei Jia
Nuoqi Chen
Tao Chen
Dongming Su
Haoming Tian
Shusen Zheng
Yifan Dai
Allan Zhao
University of Pittsburgh · USWest China Hospital of Sichuan University · CNNanjing Medical University · CNPittsburg State University · USZhejiang University · CN

Funding

Study of Leptin Receptor Deficiency in FatR01DK064383 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHAO, ALLAN Z · 2004 to 2007
$1.0M
NIDDK NIH HHS 1R01DK064383-01NIDDK NIH HHS R01 DK064383
6 · The paper itself

Abstract

objectiveTo evaluate the direct impact of n-3 polyunsaturated fatty acids (n-3 PUFAs) on the functions and viability of pancreatic beta-cells. RESEARCH DESIGN AND

methodsWe developed an mfat-1 transgenic mouse model in which endogenous production of n-3 PUFAs was achieved through overexpressing a C. elegans n-3 fatty acid desaturase gene, mfat-1. The islets and INS-1 cells expressing mfat-1 were analyzed for insulin secretion and viability in response to cytokine treatment.

resultsThe transgenic islets contained much higher levels of n-3 PUFAs and lower levels of n-6 PUFAs than the wild type. Insulin secretion stimulated by glucose, amino acids, and glucagon-like peptide-1 (GLP-1) was significantly elevated in the transgenic islets. When challenged with tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and gamma-interferon (IFN-gamma), the transgenic islets completely resisted cytokine-induced cell death. Adenoviral transduction of mfat-1 gene in wild-type islets and in INS-1 cells led to acute changes in the cellular levels of n-3- and n-6 PUFAs and recapitulated the results in the transgenic islets. The expression of mfat-1 led to decreased production of prostaglandin E(2) (PGE(2)), which in turn contributed to the elevation of insulin secretion. We further found that cytokine-induced activation of NF-kappaB and extracellular signal-related kinase 1/2 (ERK(1/2)) was significantly attenuated and that the expression of pancreatic duodenal hemeobox-1 (PDX-1), glucokinase, and insulin-1 was increased as a result of n-3 PUFA production.

conclusionsStable cellular production of n-3 PUFAs via mfat-1 can enhance insulin secretion and confers strong resistance to cytokine-induced beta-cell destruction. The utility of mfat-1 gene in deterring type 1 diabetes should be further explored in vivo.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DeathCytokinesDNA, ComplementaryDNA PrimersDNA ProbesFatty Acid DesaturasesFatty Acids, Omega-3Fatty Acids, Omega-6Genetic VectorsGlutamineInsulinInsulin-Secreting CellsInsulin SecretionCaenorhabditis elegans ProteinsCytokinesDNA, ComplementaryDNA PrimersDNA Probesfat-1 protein, C elegansFatty Acid DesaturasesFatty Acids, Omega-3Fatty Acids, Omega-6GlutamineInsulinLeucineMitogen-Activated Protein Kinase 3NF-kappa B

Identifiers

PMID19933995
PMCPMC2809969
OpenAlexW2106964014

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.