Evidence map›Paper›PMID 26160433›Full record

ArticleDiabetologia2015

Influence of endogenous NEFA on beta cell function in humans.

Eleni Rebelos, Marta Seghieri, Andrea Natali, Beverly Balkau, Alain Golay, Pier Marco Piatti, Nebojsa M Lalic, Markku Laakso, Andrea Mari, Ele Ferrannini

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 33 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

10 authors at 7 institutions in 5 countries.

Eleni RebelosDepartment of Clinical & Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy.
Marta SeghieriDepartment of Clinical & Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy.
Andrea NataliDepartment of Clinical & Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy.
Beverly BalkauInserm Unit 1018, Villejuif, France.
Alain GolayDivision of Therapeutical Teaching for Chronic Diseases, University Hospital, Geneva, Switzerland.
Pier Marco PiattiCardio-Metabolism and Clinical Trials Unit, Department of Internal Medicine, IRCCS Ospedale San Raffaele, Milan, Italy.
Nebojsa M LalicClinic for Endocrinology, Diabetes and Metabolic Diseases, CCS, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
Markku LaaksoDepartment of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland.
Andrea MariCNR Institute of Neuroscience, Padova, Italy.
Ele FerranniniDepartment of Clinical & Experimental Medicine, University of Pisa, Via Roma, 67, 56126, Pisa, Italy. ferranni@ifc.cnr.it.
University of Pisa · ITInserm · FRIRCCS Ospedale San Raffaele · ITNeuroscience Institute · ITUniversity Hospital of Geneva · CHUniversity of Belgrade · RSUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisIt is a commonly held view that chronically elevated NEFA levels adversely affect insulin secretion and insulin action (lipotoxicity). However, the effect of NEFA on beta cell function has only been explored using acute NEFA elevations. Our aim was to analyse the relationship between endogenous NEFA levels and beta cell function.

methodsIn 1,267 individuals followed-up for 3 years, we measured insulin sensitivity (by clamp) and beta cell function (by C-peptide modelling during OGTT and as the acute insulin response [AIR] to IVGTT).

resultsAt baseline, both fasting and insulin-suppressed NEFA levels were higher across glucose tolerance groups, while insulin sensitivity was lower, insulin output was higher, and beta cell glucose sensitivity and AIR were lower (all p < 0.0001). In multiple logistic analyses adjusting for age, BMI, WHR and glucose tolerance, both fasting and insulin-suppressed NEFA levels were inversely related to insulin sensitivity, as expected (both p < 0.0001). Furthermore, after adjusting for insulin sensitivity, insulin-suppressed NEFA were positively associated with total insulin output (p = 0.0042). In contrast, neither fasting nor insulin-suppressed NEFA were related to beta cell glucose sensitivity or AIR. At follow-up, worsening of glucose tolerance (n = 126) was predicted by lower insulin and beta cell glucose sensitivity. In this model, baseline NEFA were not significant predictors of progression. CONCLUSIONS/

interpretationIn the non-diabetic state and in subjects with impaired glucose tolerance, circulating endogenous NEFA are not independently associated measures of beta cell function, and do not predict deterioration of glucose tolerance. Thus, in the Relationship Between Insulin Sensitivity and Cardiovascular Disease (RISC) cohort there is no evidence for beta cell lipotoxicity of endogenous total NEFA concentrations.

Indexed as

AdultBlood GlucoseFatty Acids, NonesterifiedFemaleGlucose IntoleranceHumansInsulinInsulin ResistanceInsulin-Secreting CellsMaleMiddle AgedBlood GlucoseFatty Acids, NonesterifiedInsulinBeta cell functionBeta cell glucose sensitivityGlucose intoleranceInsulin resistanceLipotoxicityNEFA

Identifiers

PMID26160433
OpenAlexW1601942514

What OpenQuestion holds

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Registered trials

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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.