Evidence map›Paper›PMID 8904921›Full record

ReviewActa diabetologica1996

Regulation, perturbation, and correction of metabolic events in pancreatic islets.

W J Malaisse

Abstract readReview
PubMed Publisher
In one paragraph

Review in Acta diabetologica, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

0 citing papers in PubMed, 6 citations in OpenAlex.

No citing paper in PubMed yet.

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

1 author.

W J MalaisseLaboratory of Experimental Medicine, Brussels Free University, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The physiological regulation of nutrient catabolism in islet cells, its perturbation in non-insulin-dependent diabetes mellitus, and the tools available to compensate for such a perturbation are reviewed. In terms of physiology, emphasis is placed on the relevance of glucokinase to hexose-induced insulin release, protein-to-protein interaction and enzyme-to-enzyme channelling, and the preferential stimulation of mitochondrial oxidative events in glucose-stimulated B-cells. In terms of pathology, attention is drawn to the deficiency of FAD-linked mitochondrial glycerophosphate dehydrogenase. Last, as far as therapeutic aspects are concerned, the potential usefulness of hypoglycemic sulfonylureas and meglitinide analogs, adenosine analogs, non-glucidic nutrients, and GLP-1 is underlined.

Indexed as

AdenosineAnimalsDiabetes Mellitus, Type 2GlucagonGlucagon-Like Peptide 1GlucokinaseGlycerolphosphate DehydrogenaseHexosesHomeostasisHumansHypoglycemic AgentsInsulinInsulin SecretionIslets of LangerhansMitochondriaOxidative PhosphorylationAdenosineGlucagonGlucagon-Like Peptide 1GlucokinaseGlycerolphosphate DehydrogenaseHexosesHypoglycemic AgentsInsulinPeptide FragmentsProtein PrecursorsSulfonylurea Compounds

Identifiers

PMID8904921
OpenAlexW2024479144

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.