Evidence map›Paper›PMID 26221611›Full record

ArticleJournal of diabetes research2015

Effects of High Glucose Levels and Glycated Serum on GIP Responsiveness in the Pancreatic Beta Cell Line HIT-T15.

Alessandra Puddu, Roberta Sanguineti, Fabrizio Montecucco, Giorgio Luciano Viviani

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
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

4 authors at 2 institutions in 2 countries.

Alessandra PudduDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV, 16143 Genoa, Italy.
Roberta SanguinetiDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV, 16143 Genoa, Italy.
Fabrizio MontecuccoDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV, 16143 Genoa, Italy ; Division of Cardiology, Department of Medicine, Geneva University Hospitals, Faculty of Medicine, Foundation for Medical Researches, 64 Avenue de la Roseraie, 1211 Geneva, Switzerland ; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 4 Rue Gabrielle-Perret-Gentil, 1205 Geneva, Switzerland.
Giorgio Luciano VivianiDepartment of Internal Medicine, University of Genoa, Viale Benedetto XV, 16143 Genoa, Italy.
University of Genoa · ITUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-dependent insulinotropic peptide (GIP) is an incretin hormone produced in the gastrointestinal tract that stimulates glucose dependent insulin secretion. Impaired incretin response has been documented in diabetic patients and was mainly related to the inability of the pancreatic beta cells to secrete insulin in response to GIP. Advanced Glycation End Products (AGEs) have been shown to play an important role in pancreatic beta cell dysfunction. The aim of this study is to investigate whether the exposure to AGEs can induce GIP resistance in the pancreatic beta cell line HIT-T15. Cells were cultured for 5 days in low (CTR) or high glucose (HG) concentration in the presence of AGEs (GS) to evaluate the expression of GIP receptor (GIPR), the intracellular signaling activated by GIP, and secretion of insulin in response to GIP. The results showed that incubation with GS alone altered intracellular GIP signaling and decreased insulin secretion as compared to CTR. GS in combination with HG reduced the expression of GIPR and PI3K and abrogated GIP-induced AKT phosphorylation and GIP-stimulated insulin secretion. In conclusion, we showed that treatment with GS is associated with the loss of the insulinotropic effect of GIP in hyperglycemic conditions.

Indexed as

Down-RegulationAnimalsBlood GlucoseBlotting, WesternCell LineGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Glycation End Products, AdvancedHumansHyperglycemiaInsulinInsulin-Secreting CellsInsulin SecretionMesocricetusPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsBlood GlucoseGastric Inhibitory Polypeptidegastric inhibitory polypeptide receptorGlucagon-Like Peptide 1Glycation End Products, AdvancedInsulinPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, Gastrointestinal HormoneRecombinant Proteins

Identifiers

PMID26221611
PMCPMC4499629
OpenAlexW1573295743

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.