Evidence map›Paper›PMID 22349073›Full record

ArticleDiabetologia2012

Fasting and oral glucose-stimulated levels of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are highly familial traits.

A P Gjesing, C T Ekstrøm, H Eiberg, S A Urhammer, J J Holst, O Pedersen, T Hansen

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In one paragraph

Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Genome-Wide Association Analysis of Pancreatic Beta-Cell Glucose Sensitivity.The Journal of clinical endocrinology and metabolism · 2021
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  8. Structural basis for GLP-1 receptor activation by LY3502970, an orally active nonpeptide agonist.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 3 institutions in 1 country.

A P GjesingNovo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, University of Copenhagen, Universitetsparken 1, DK-2100 Copenhagen, Denmark. anette.gjesing@sund.ku.dk
C T Ekstrøm
H Eiberg
S A Urhammer
J J Holst
O Pedersen
T Hansen
University of Copenhagen · DKNovo Nordisk Foundation · DKFrederiksberg Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisHeritability estimates have shown a varying degree of genetic contribution to traits related to type 2 diabetes. Therefore, the objective of this study was to investigate the familiality of fasting and stimulated measures of plasma glucose, serum insulin, serum C-peptide, plasma glucose-dependent insulinotropic polypeptide (GIP) and plasma glucagon-like peptide-1 (GLP-1) among non-diabetic relatives of Danish type 2 diabetic patients.

methodsSixty-one families comprising 193 non-diabetic offspring, 29 non-diabetic spouses, 72 non-diabetic relatives (parent, sibling, etc.) and two non-related relatives underwent a 4 h 75 g OGTT with measurements of plasma glucose, serum insulin, serum C-peptide, plasma GIP and plasma GLP-1 levels at 18 time points. Insulin secretion rates (ISR) and beta cell responses to glucose, GIP and GLP-1 were calculated. Familiality was estimated based on OGTT-derived measures.

resultsA high level of familiality was observed during the OGTT for plasma levels of GIP and GLP-1, with peak familiality values of 74 ± 16% and 65 ± 15%, respectively (h (2) ± SE). Familiality values were lower for plasma glucose, serum insulin and serum C-peptide during the OGTT (range 8-48%, 14-44% and 15-61%, respectively). ISR presented the highest familiality value at fasting reaching 59 ± 16%. Beta cell responsiveness to glucose, GLP-1 and GIP also revealed a strong genetic influence, with peak familiality estimates of 62 ± 13%, 76 ± 15% and 70 ± 14%, respectively. CONCLUSIONS/

interpretationOur results suggest that circulating levels of GIP and GLP-1 as well as beta cell response to these incretins are highly familial compared with more commonly investigated measures of glucose homeostasis such as fasting and stimulated plasma glucose, serum insulin and serum C-peptide.

Indexed as

FastingAdultAgedAged, 80 and overBlood GlucoseC-PeptideDenmarkDiabetes Mellitus, Type 2FemaleGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Glucose Tolerance TestHumansInsulinInsulin-Secreting CellsInsulin SecretionBlood GlucoseC-PeptideGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Insulin

Identifiers

PMID22349073
OpenAlexW2067059221

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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.