Evidence map›Paper›PMID 29093273›Full record

SynthesisJCI insight2017

Genetic determinants of circulating GIP and GLP-1 concentrations.

Peter Almgren, Andreas Lindqvist, Ulrika Krus, Liisa Hakaste, Emilia Ottosson-Laakso, Olof Asplund, Emily Sonestedt, Rashmi B Prasad, Esa Laurila, Marju Orho-Melander and 7 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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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

17 authors at 4 institutions in 3 countries.

Peter AlmgrenLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Andreas LindqvistLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Ulrika KrusLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Liisa HakasteEndocrinology, Abdominal Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Diabetes and Obesity Research Program, University of Helsinki and Folkhälsan Research Center, Helsinki, Finland.
Emilia Ottosson-LaaksoLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Olof AsplundLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Emily SonestedtLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Rashmi B PrasadLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Esa LaurilaLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Marju Orho-MelanderLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Olle MelanderLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Tiinamaija TuomiEndocrinology, Abdominal Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Diabetes and Obesity Research Program, University of Helsinki and Folkhälsan Research Center, Helsinki, Finland.
Jens Juul HolstNovo Nordisk Foundation Center for Basic Metabolic Research and Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Peter M NilssonClinical Research Unit Medicine, Department of Internal Medicine, and Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Nils WierupLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Leif GroopLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Emma AhlqvistLund University Diabetes Centre, Department of Clinical Sciences, Malmö, Lund University, Skåne University Hospital, Malmö, Sweden.
Lund University · SEUniversity of Helsinki · FIMalmö University · SEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The secretion of insulin and glucagon from the pancreas and the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) from the gastrointestinal tract is essential for glucose homeostasis. Several novel treatment strategies for type 2 diabetes (T2D) mimic GLP-1 actions or inhibit incretin degradation (DPP4 inhibitors), but none is thus far aimed at increasing the secretion of endogenous incretins. In order to identify new potential therapeutic targets for treatment of T2D, we performed a meta-analysis of a GWAS and an exome-wide association study of circulating insulin, glucagon, GIP, and GLP-1 concentrations measured during an oral glucose tolerance test in up to 7,828 individuals. We identified 6 genome-wide significant functional loci associated with plasma incretin concentrations in or near the SLC5A1 (encoding SGLT1), GIPR, ABO, GLP2R, F13A1, and HOXD1 genes and studied the effect of these variants on mRNA expression in pancreatic islet and on metabolic phenotypes. Immunohistochemistry showed expression of GIPR, ABO, and HOXD1 in human enteroendocrine cells and expression of ABO in pancreatic islets, supporting a role in hormone secretion. This study thus provides candidate genes and insight into mechanisms by which secretion and breakdown of GIP and GLP-1 are regulated.

Indexed as

Genetic VariationABO Blood-Group SystemAgedAged, 80 and overDiabetes Mellitus, Type 2Dipeptidyl Peptidase 4Enteroendocrine CellsFemaleGastric Inhibitory PolypeptideGastrointestinal HormonesGastrointestinal TractGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-2 ReceptorGlucoseGlucose Tolerance TestABO Blood-Group SystemDipeptidyl Peptidase 4DPP4 protein, humanGastric Inhibitory Polypeptidegastric inhibitory polypeptide receptorGastrointestinal HormonesGLP2R protein, humanGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-2 ReceptorGlucoseHomeodomain ProteinsHOXD1 protein, humanIncretinsInsulinReceptors, Gastrointestinal HormoneRNA, MessengerSLC5A1 protein, humanSodium-Glucose Transporter 1

Identifiers

PMID29093273
PMCPMC5963138
OpenAlexW2766177815

What OpenQuestion holds

Textmetadata
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.