Evidence map›Paper›PMID 20231880›Full record

ArticlePloS one2010

A GIP receptor agonist exhibits beta-cell anti-apoptotic actions in rat models of diabetes resulting in improved beta-cell function and glycemic control.

Scott B Widenmaier, Su-Jin Kim, Gary K Yang, Thomas De Los Reyes, Cuilan Nian, Ali Asadi, Yutaka Seino, Timothy J Kieffer, Yin Nam Kwok, Christopher H S McIntosh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
9.8field-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

36 citing papers in PubMed, 100 citations in OpenAlex.

  1. Revitalizing GIP: Therapeutic Potential in Metabolic and Neurodegenerative Disorders.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
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  11. Mechanisms of Cardiorenal Protection of Glucagon-Like Peptide-1 Receptor Agonists.Advances in chronic kidney disease · 2021 · on this map
    Review
  12. Incretins in obesity and diabetes.Annals of the New York Academy of Sciences · 2020
    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

10 authors at 2 institutions in 2 countries.

Scott B WidenmaierDepartment of Cellular and Physiological Sciences and the Diabetes Research Group, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia, Canada.
Su-Jin Kim
Gary K Yang
Thomas De Los Reyes
Cuilan Nian
Ali Asadi
Yutaka Seino
Timothy J Kieffer
Yin Nam Kwok
Christopher H S McIntosh
University of British Columbia · CAKansai Electric Power Hospital · JP

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

aimsThe gastrointestinal hormone GIP promotes pancreatic islet function and exerts pro-survival actions on cultured beta-cells. However, GIP also promotes lipogenesis, thus potentially restricting its therapeutic use. The current studies evaluated the effects of a truncated GIP analog, D-Ala(2)-GIP(1-30) (D-GIP(1-30)), on glucose homeostasis and beta-cell mass in rat models of diabetes. MATERIALS AND

methodsThe insulinotropic and pro-survival potency of D-GIP(1-30) was evaluated in perfused pancreas preparations and cultured INS-1 beta-cells, respectively, and receptor selectivity evaluated using wild type and GIP receptor knockout mice. Effects of D-GIP(1-30) on beta-cell function and glucose homeostasis, in vivo, were determined using Lean Zucker rats, obese Vancouver diabetic fatty rats, streptozotocin treated rats, and obese Zucker diabetic fatty rats, with effects on beta-cell mass determined in histological studies of pancreatic tissue. Lipogenic effects of D-GIP(1-30) were evaluated on cultured 3T3-L1 adipocytes.

resultsAcutely, D-GIP(1-30) improved glucose tolerance and insulin secretion. Chronic treatment with D-GIP(1-30) reduced levels of islet pro-apoptotic proteins in Vancouver diabetic fatty rats and preserved beta-cell mass in streptozotocin treated rats and Zucker diabetic fatty rats, resulting in improved insulin responses and glycemic control in each animal model, with no change in body weight. In in vitro studies, D-GIP(1-30) exhibited equivalent potency to GIP(1-42) on beta-cell function and survival, but greatly reduced action on lipoprotein lipase activity in 3T3-L1 adipocytes.

conclusionsThese findings demonstrate that truncated forms of GIP exhibit potent anti-diabetic actions, without pro-obesity effects, and that the C-terminus contributes to the lipogenic actions of GIP.

Indexed as

Apoptosis3T3 CellsAdipocytesAnimalsApoptosis Regulatory ProteinsDiabetes Mellitus, ExperimentalGlucoseGlucose Tolerance TestInsulin-Secreting CellsMiceMice, Inbred C57BLMice, KnockoutRatsRats, ZuckerReceptors, Gastrointestinal HormoneApoptosis Regulatory Proteinsgastric inhibitory polypeptide receptorGlucoseReceptors, Gastrointestinal Hormone

Identifiers

PMID20231880
PMCPMC2834736
OpenAlexW2054867747

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.