Evidence map›Paper›PMID 16781373›Full record

ArticleJournal of the American College of Cardiology2006

Family history of diabetes is a major determinant of endothelial function.

Allison B Goldfine, Joshua A Beckman, Rebecca A Betensky, Heather Devlin, Shauna Hurley, Nerea Varo, Uwe Schonbeck, Mary Elizabeth Patti, Mark A Creager

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Journal of the American College of Cardiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02633488 (Effect of Metformin on Insulin Sensitivity and Pan-Arterial Vascular Function in Adults With Metabolic Syndrome), which is not on this map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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.

NCT02633488 nacompletedstarted 2014, after this paper: background citation

Effect of Metformin on Insulin Sensitivity and Pan-Arterial Vascular Function in Adults With Metabolic Syndrome

Ran2014Enrolled19Registered outcomes1Posted comparisons1ConditionsInsulin Sensitivity, Metabolic SyndromeArmsMetformin, Placebos
Open the trial in the graph
3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  5. Article
  6. Gut microbiota and obesity: New insights.Frontiers in nutrition · 2022
    Review
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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

9 authors at 3 institutions in 1 country.

Allison B GoldfineJoslin Diabetes Center, Boston, Massachusetts 02215, USA. allison.goldfine@joslin.harvard.edu
Joshua A Beckman
Rebecca A Betensky
Heather Devlin
Shauna Hurley
Nerea Varo
Uwe Schonbeck
Mary Elizabeth Patti
Mark A Creager
Brigham and Women's Hospital · USJoslin Diabetes Center · USHarvard University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
ZINC STATUS AND T CELL DISORDER IN MILD HUMAN ZINC DEFICIENCYM01RR001032 · NCRR · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 1985 to 2008
$32.3M
Tissue AnalysesP01HL048743 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MICHEL, THOMAS · 1992 to 2014
$26.3M
PHYSIOLOGY AND MOLECULAR DETERMINANTS OF DIABETESK23DK002795 · NIDDK · JOSLIN DIABETES CENTER · PI GOLDFINE, ALLISON B · 2000 to 2004
$621k
NCRR NIH HHS M01 RR001032NHLBI NIH HHS P01 HL48743NIDDK NIH HHS K23-DK02795NIDDK NIH HHS P30 DK36836
6 · The paper itself

Abstract

objectivesWe evaluated whether endothelial dysfunction was present in nondiabetic persons with a family history (FH) of diabetes and assessed its relationship with insulin resistance and atherosclerosis risk factors.

backgroundAtherosclerosis is frequently present when type 2 diabetes (T2D) is first diagnosed. Endothelial dysfunction contributes to atherogenesis.

methodsOral glucose tolerance and brachial artery flow-mediated, endothelium-dependent vasodilation (EDV) were assessed in 38 nondiabetic subjects; offspring of two parents with T2D (FH+) or with no first-degree relative with diabetes (FH-).

resultsAlthough fasting glucose was higher in FH+ than FH- (5.3 +/- 0.1 mmol/l vs. 4.9 +/- 0.1 mmol/l, p < 0.03), glycemic burden assessed as 2-h or area-under-the-curve glucose after glucose load or glycosylated hemoglobin (HbA1c), and measures of insulin sensitivity or inflammation did not differ. Brachial artery flow-mediated EDV was reduced in FH+ (7.1 +/- 0.9% vs. 11.7 +/- 1.6%, p < 0.02), with no difference in nitroglycerin-induced endothelium-independent vasodilatation. In the combined cohort, only FH+ (r2 = 0.12, p < 0.02) and HbA1c (r2 = 0.14, p < 0.02) correlated with EDV. Insulin resistance, assessed by tertile of homeostasis model assessment of insulin resistance (HOMA-IR), was associated with impaired endothelium-dependent vasodilatation in FH- (p < 0.03, analysis of variance), but not in FH+, as even the most insulin-sensitive FH+ offspring had diminished endothelial function. In multiple regression analysis, including established cardiac risk factors, blood pressure and lipids, HbA1c, and HOMA-IR, FH remained a significant determinant of EDV (p = 0.04).

conclusionsBioavailability of nitric oxide is lower in persons with a strong FH of T2D. Glycemic burden, even in the nondiabetic range, can contribute to endothelial dysfunction. Abnormalities of endothelial function may contribute to atherosclerosis before development of overt diabetes.

Indexed as

AdultDiabetes Mellitus, Type 2Endothelium, VascularFemaleHeart DiseasesHumansInsulin ResistanceMaleRisk FactorsVasodilation

Identifiers

PMID16781373
OpenAlexW2051893892

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.