Evidence map›Paper›PMID 26417659›Full record

ArticleNutrition & diabetes2015

Plasma IL-1Ra: linking hyperapoB to risk factors for type 2 diabetes independent of obesity in humans.

S Bissonnette, N Saint-Pierre, V Lamantia, Y Cyr, H Wassef, M Faraj

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Nutrition & diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04496154 (The Inflammasome and Dysfunctional Adipose Tissue), which is not on this map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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.

NCT04496154 nacompletednot on this map

The Inflammasome and Dysfunctional Adipose Tissue: Why Should apoB-lipoproteins be Targeted in Humans

TypeinterventionalSponsorMay Faraj, PDt, PhDRan2013 to 2020Enrolled41ConditionsType 2 Diabetes, Insulin Sensitivity/Resistance, Inflammatory Response, Fatty Acids, Omega-3ArmsOmega-3 fatty acids (2.7 g/d, EPA:DHA, 2:1)
3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 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

6 authors at 1 institution in 1 country.

S BissonnetteFaculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
N Saint-PierreDépartement de Nutrition, Institut de Recherches Cliniques de Montréal (IRCM), Montréal, Québec, Canada.
V LamantiaFaculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
Y CyrFaculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
H WassefFaculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
M FarajFaculty of Medicine, Université de Montréal, Montréal, Québec, Canada.
Montreal Clinical Research Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivePlasma apoB predicts the incidence of type 2 diabetes (T2D); however, the link between apoB-linpoproteins and risks for T2D remain unclear. Insulin resistance (IR) and compensatory hyperinsulinemia characterize prediabetes, and the involvement of an activated interleukin-1 (IL-1) family, mainly IL-1β and its receptor antagonist (IL-Ra), is well documented. ApoB-lipoproteins were reported to promote IL-1β secretion in immune cells; however, in vivo evidence is lacking. We hypothesized that obese subjects with hyperapoB have an activated IL-1 system that explains hyperinsulinemia and IR in these subjects. SUBJECTS/

methodsWe examined 81 well-characterized normoglycemic men and postmenopausal women (⩾27 kg m(-2), 45-74 years, non-smokers, sedentary, free of chronic disease). Insulin secretion and sensitivity were measured by the gold-standard Botnia clamp, which is a combination of a 1-h intravenous glucose tolerance test (IVGTT) followed by 3-h hyperinsulinemic euglycemic clamp.

resultsPlasma IL-1β was near detection limit (0.071-0.216 pg ml(-1)), while IL-1Ra accumulated at 1000-folds higher (77-1068 pg ml(-1)). Plasma apoB (0.34-1.80 g l(-1)) associated significantly with hypersinsulinemia (totalIVGTT: C-peptide r=0.27, insulin r=0.22), IR (M/I=-0.29) and plasma IL-1Ra (r=0.26) but not with IL-1β. Plasma IL-1Ra associated with plasma IL-1β (r=0.40), and more strongly with hyperinsulinemia and IR than apoB, while the association of plasma IL-1β was limited to second phase and total insulin secretion (r=0.23). Adjusting the association of plasma apoB to hyperinsulinemia and IR for IL-1Ra eliminated these associations. Furthermore, despite equivalent body composition, subjects with hyperapoB (⩾80th percentile, 1.14 g l(-1)) had higher C-peptide secretion and lower insulin sensitivity than those with low plasma apoB (⩽20th percentile, 0.78 g l(-1)). Adjustment for plasma IL-1 Ra eliminated all group differences.

conclusionPlasma apoB is associated with hyperinsulinemia and IR in normoglycemic obese subjects, which is eliminated upon adjustment for plasma IL-1Ra. This may implicate the IL-1 family in elevated risks for T2D in obese subjects with hyperapoB.

Identifiers

PMID26417659
PMCPMC4657760
OpenAlexW2193233774

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Registered trials

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.