Evidence map›Paper›PMID 18048763›Full record

ReviewEndocrine reviews2008

Glucolipotoxicity: fuel excess and beta-cell dysfunction.

Vincent Poitout, R Paul Robertson

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrine reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 522 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
522citing papers in PubMed, 2 pooled it
70.5field-weighted citation impact, top 1% 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

522 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,056 citations in OpenAlex.

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462 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

2 authors at 2 institutions in 2 countries.

Vincent PoitoutMontreal Diabetes Research Center, CR-CHUM, Technopole Angus, 2901 Rachel Est, Montreal, Quebec, Canada H1W 4A4. vincent.poitout@umontreal.ca
R Paul Robertson
Pacific Northwest Diabetes Research Institute · USUniversity of Washington · US

Funding

Neutral lipid dysregulation of the pancreatic beta-cellR01DK058096 · NIDDK · UNIVERSITY OF MONTREAL HOSPITAL · PI POITOUT, VINCENT · 2001 to 2020
$3.9M
PGE RECEPTOR - LIVER AND FAT METABOLISMR01DK038325 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ROBERTSON, RODERICK PAUL · 1986 to 2010
$3.6M
CIHR 77686NIDDK NIH HHS R01 DK038325NIDDK NIH HHS R01 DK058096NIDDK NIH HHS R01-DK38325NIDDK NIH HHS R01-DK58096
6 · The paper itself

Abstract

Glucotoxicity, lipotoxicity, and glucolipotoxicity are secondary phenomena that are proposed to play a role in all forms of type 2 diabetes. The underlying concept is that once the primary pathogenesis of diabetes is established, probably involving both genetic and environmental forces, hyperglycemia and very commonly hyperlipidemia ensue and thereafter exert additional damaging or toxic effects on the beta-cell. In addition to their contribution to the deterioration of beta-cell function after the onset of the disease, elevations of plasma fatty acid levels that often accompany insulin resistance may, as glucose levels begin to rise outside of the normal range, also play a pathogenic role in the early stages of the disease. Because hyperglycemia is a prerequisite for lipotoxicity to occur, the term glucolipotoxicity, rather than lipotoxicity, is more appropriate to describe deleterious effects of lipids on beta-cell function. In vitro and in vivo evidence supporting the concept of glucotoxicity is presented first, as well as a description of the underlying mechanisms with an emphasis on the role of oxidative stress. Second, we discuss the functional manifestations of glucolipotoxicity on insulin secretion, insulin gene expression, and beta-cell death, and the role of glucose in the mechanisms of glucolipotoxicity. Finally, we attempt to define the role of these phenomena in the natural history of beta-cell compensation, decompensation, and failure during the course of type 2 diabetes.

Indexed as

AnimalsDiabetes Mellitus, Type 2Energy MetabolismGlucoseHumansInsulin-Secreting CellsLipid MetabolismGlucose

Identifiers

PMID18048763
PMCPMC2528858
OpenAlexW2082515526

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.