Evidence map›Paper›PMID 25463099›Full record

ArticleAtherosclerosis2014

Joint effect of insulin signaling genes on all-cause mortality.

Claudia Menzaghi, Andrea Fontana, Massimiliano Copetti, Stefano Rizza, Belinda Spoto, Patinut Buranasupkajorn, Giovanni Tripepi, Antonella Marucci, Diego Bailetti, Timothy Hastings and 9 more

Abstract read
In one paragraph

Article in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. 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

19 authors.

Claudia MenzaghiResearch Unit of Diabetes and Endocrine Diseases IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. Electronic address: c.menzaghi@operapadrepio.it.
Andrea FontanaUnit of Biostatistics IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Massimiliano CopettiUnit of Biostatistics IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Stefano RizzaDepartment of Internal Medicine, University of Rome Tor Vergata, Rome, Italy.
Belinda SpotoCNR-IBIM, Research Unit of Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
Patinut BuranasupkajornResearch Division, Joslin Diabetes Center, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA.
Giovanni TripepiCNR-IBIM, Research Unit of Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
Antonella MarucciResearch Unit of Diabetes and Endocrine Diseases IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Diego BailettiIRCSS Casa Sollievo della Sofferenza-Mendel Laboratory, Rome, Italy; Department of Experimental Medicine, Sapienza University of Rome, Italy.
Timothy HastingsResearch Division, Joslin Diabetes Center, Boston, MA, USA.
Alessandra TestaCNR-IBIM, Research Unit of Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
Christine MendoncaResearch Division, Joslin Diabetes Center, Boston, MA, USA.
Francesca MallamaciCNR-IBIM, Research Unit of Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
Salvatore De CosmoUnit of Endocrinology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Simonetta BacciUnit of Endocrinology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Massimo FedericiDepartment of Internal Medicine, University of Rome Tor Vergata, Rome, Italy.
Alessandro DoriaResearch Division, Joslin Diabetes Center, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA.
Carmine ZoccaliCNR-IBIM, Research Unit of Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
Vincenzo TrischittaResearch Unit of Diabetes and Endocrine Diseases IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy; Department of Experimental Medicine, Sapienza University of Rome, Italy. Electronic address: vincenzo.trischitta@uniroma1.it.

Funding

Variability in Adipokine Genes and AtherosclerosisR01HL073168 · NHLBI · JOSLIN DIABETES CENTER · PI DORIA, ALESSANDRO · 2003 to 2012
$5.8M
Genetic modifiers of the effect of intensive glycemic control on CVD riskR01HL110400 · NHLBI · JOSLIN DIABETES CENTER · PI DORIA, ALESSANDRO · 2011 to 2014
$3.8M
NHLBI NIH HHS R01 HL073168NHLBI NIH HHS R01 HL110400NIDDK NIH HHS DK110400NIDDK NIH HHS R01 DK073168
6 · The paper itself

Abstract

objectiveWe have previously reported the combined effect of SNPs perturbing insulin signaling (ENPP1 K121Q, rs1044498; IRS1 G972R, rs1801278; TRIB3 Q84R, rs2295490) on insulin resistance (IR), type 2 diabetes (T2D) and cardiovascular events. We here investigated whether such a combined effect affects also all-cause mortality in a sample of 1851 Whites of European ancestry.

methodsWe investigated a first sample of 721 patients, 232 deaths, 3389 person-years (py). Replication was assessed in two samples of patients with T2D: the Gargano Mortality Study (GMS) of 714 patients, 127 deaths, 5426 py and the Joslin Kidney Study (JKS) comprising 416 patients, 214 deaths, 5325 py.

resultsIn the first sample, individuals carrying 1 or ≥ 2 risk alleles had 33% (p = 0.06) and 51% (p = 0.02) increased risk of mortality, as compared with individuals with no risk alleles. A similar, though not significant, trend was obtained in the two replication samples only for subject carrying ≥ 2 risk alleles. In a pooled analysis, individuals carrying ≥ 2 risk alleles had higher mortality rate as compared to those carrying 0 risk alleles (HR = 1.34, 95%CI = 1.08-1.67; p = 0.008), and as compared to those carrying only one risk allele (HR = 1.41, 95%CI = 1.13-1.75; p = 0.002). This association was independent from several possible confounders including sex, age, BMI, hypertension and diabetes status.

conclusionOur data suggest that variants affecting insulin signaling exert a joint effect on all-cause mortality and is consistent with a role of abnormal insulin signaling on mortality risk.

Indexed as

MortalityAgedAllelesAtherosclerosisCardiovascular DiseasesDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeHumansInsulinInsulin ResistanceItalyMaleMiddle AgedInsulinENPP1IRS1Prospective studyTRIB3

Identifiers

PMID25463099
PMCPMC4294190

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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.