Evidence map›Paper›PMID 20547980›Full record

ArticleDiabetes2010

Beta-cell failure in diet-induced obese mice stratified according to body weight gain: secretory dysfunction and altered islet lipid metabolism without steatosis or reduced beta-cell mass.

Marie-Line Peyot, Emilie Pepin, Julien Lamontagne, Martin G Latour, Bader Zarrouki, Roxane Lussier, Marco Pineda, Thomas L Jetton, S R Murthy Madiraju, Erik Joly and 1 more

Open access · bronzeAbstract 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 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 2% 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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Article
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  19. Nutrients · 2020
    Article
  20. Article

41 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 2 institutions in 2 countries.

Marie-Line PeyotMontreal Diabetes Research Center and CRCHUM, Montreal, QC, Canada. marie-line.peyot@crchum.qc.ca.
Emilie Pepin
Julien Lamontagne
Martin G Latour
Bader Zarrouki
Roxane Lussier
Marco Pineda
Thomas L Jetton
S R Murthy Madiraju
Erik Joly
Marc Prentki
Université de Montréal · CAUniversity of Vermont · US

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

objectiveC57Bl/6 mice develop obesity and mild hyperglycemia when fed a high-fat diet (HFD). Although diet-induced obesity (DIO) is a widely studied model of type 2 diabetes, little is known about beta-cell failure in these mice. RESEARCH DESIGN AND

methodsDIO mice were separated in two groups according to body weight gain: low- and high-HFD responders (LDR and HDR). We examined whether mild hyperglycemia in HDR mice is due to reduced beta-cell mass or function and studied islet metabolism and signaling.

resultsHDR mice were more obese, hyperinsulinemic, insulin resistant, and hyperglycemic and showed a more altered plasma lipid profile than LDR. LDR mice largely compensated insulin resistance, whereas HDR showed perturbed glucose homeostasis. Neither LDR nor HDR mice showed reduced beta-cell mass, altered islet glucose metabolism, and triglyceride deposition. Insulin secretion in response to glucose, KCl, and arginine was impaired in LDR and almost abolished in HDR islets. Palmitate partially restored glucose- and KCl-stimulated secretion. The glucose-induced rise in ATP was reduced in both DIO groups, and the glucose-induced rise in Ca(2+) was reduced in HDR islets relatively to LDR. Glucose-stimulated lipolysis was decreased in LDR and HDR islets, whereas fat oxidation was increased in HDR islets only. Fatty acid esterification processes were markedly diminished, and free cholesterol accumulated in HDR islets.

conclusionsbeta-Cell failure in HDR mice is not due to reduced beta-cell mass and glucose metabolism or steatosis but to a secretory dysfunction that is possibly due to altered ATP/Ca(2+) and lipid signaling, as well as free cholesterol deposition.

Indexed as

Adenosine TriphosphateAnimalsCell DivisionDietDietary FatsGlucoseGlucose Clamp TechniqueInsulinInsulin-Secreting CellsIslets of LangerhansLipolysisMaleMiceMice, Inbred C57BLObesityProinsulinAdenosine TriphosphateDietary FatsGlucoseInsulinProinsulin

Identifiers

PMID20547980
PMCPMC2927940
OpenAlexW2129505260

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.