Evidence map›Paper›PMID 19276444›Full record

Trial reportDiabetes2009

Exogenous glucose-dependent insulinotropic polypeptide worsens post prandial hyperglycemia in type 2 diabetes.

Chee W Chia, Olga D Carlson, Wook Kim, Yu-Kyong Shin, Cornelia P Charles, Hee Seung Kim, Denise L Melvin, Josephine M Egan

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 168 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. GIP contributes to islet trihormonal abnormalities in type 2 diabetes.The Journal of clinical endocrinology and metabolism · 2014
    Trial
  5. Trial
  6. Trial
  7. Trial
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  9. Review
  10. Article
  11. Pan-hypoileism: an endocrine disease.Einstein (Sao Paulo, Brazil) · 2026
    Review
  12. Revitalizing GIP: Therapeutic Potential in Metabolic and Neurodegenerative Disorders.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

18 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

8 authors at 3 institutions in 1 country.

Chee W ChiaNational Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA.
Olga D Carlson
Wook Kim
Yu-Kyong Shin
Cornelia P Charles
Hee Seung Kim
Denise L Melvin
Josephine M Egan
National Institute on Aging · USNational Institutes of Health · USInstitute on Aging · US

Funding

Drug Development of GLP-1 receptor agonistsZIAAG000905 · NIA · NATIONAL INSTITUTE ON AGING · PI EARLEY, JOSEPHINE · 2009 to 2019
$4.6M
EXENDIN-4 AS A TREATMENT FOR DIABETES MELLITUSZ01AG000905 · NIA · NATIONAL INSTITUTE ON AGING · PI EGAN, JOSEPHINE M · 1997 to 2008
$1.5M
Intramural NIH HHS
6 · The paper itself

Abstract

objectiveGlucose-dependent insulinotropic polypeptide (GIP), unlike glucagon-like peptide (GLP)-1, lacks glucose-lowering properties in patients with type 2 diabetes. We designed this study to elucidate the underlying pathophysiology. RESEARCH DESIGN AND

methodsTwenty-two insulin-naïve subjects with type 2 diabetes were given either synthetic human GIP (20 ng x kg(-1) x min(-1)) or placebo (normal saline) over 180 min, starting with the first bite of a mixed meal (plus 1 g of acetaminophen) on two separate occasions. Frequent blood samples were obtained over 6 h to determine plasma GIP, GLP-1, glucose, insulin, glucagon, resistin, and acetaminophen levels.

resultsCompared with placebo, GIP induced an early postprandial increase in insulin levels. Intriguingly, GIP also induced an early postprandial augmentation in glucagon, a significant elevation in late postprandial glucose, and a decrease in late postprandial GLP-1 levels. Resistin and acetaminophen levels were comparable in both interventions. By immunocytochemistry, GIP receptors were present on human and mouse alpha-cells. In alphaTC1 cell line, GIP induced an increase in intracellular cAMP and glucagon secretion. CONCLUSIONS; GIP, given to achieve supraphysiological plasma levels, still had an early, short-lived insulinotropic effect in type 2 diabetes. However, with a concomitant increase in glucagon, the glucose-lowering effect was lost. GIP infusion further worsened hyperglycemia postprandially, most likely through its suppressive effect on GLP-1. These findings make it unlikely that GIP or GIP receptor agonists will be useful in treating the hyperglycemia of patients with type 2 diabetes.

Indexed as

Area Under CurveBlood GlucoseCross-Over StudiesCyclic AMPDiabetes Mellitus, Type 2Diet, DiabeticGlucagonGlutaminaseHumansHyperglycemiaHypoglycemic AgentsImmunohistochemistryIntracellular Signaling Peptides and ProteinsMetforminPlacebosPostprandial PeriodBlood GlucoseCyclic AMPGlucagonGlutaminaseHypoglycemic AgentsIntracellular Signaling Peptides and ProteinsMetforminPlacebosSulfonylurea CompoundsTAX1BP3 protein, human

Identifiers

PMID19276444
PMCPMC2682676
OpenAlexW2113527429

What OpenQuestion holds

Texttitle and abstract
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.