Linked Life Data

15636429

Source:http://linkedlifedata.com/resource/pubmed/id/15636429

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-1-7
pubmed:abstractText
Several association studies have indicated the insulin receptor substrate-1 (IRS-1) gene G972R variant as a genetic risk factor for insulin resistance, particularly in presence of obesity. A few studies have also suggested a possible effect of the G972R variant on insulin secretion. The aim of this study was to evaluate the role of the IRS-1 gene G972R variant in 61 subjects with "uncomplicated" obesity [i.e. without diabetes, hypertension, dyslipidemia, coronary artery disease (CAD)], studied by hyperinsulinemic-euglycemic clamp. The presence of the G972R variant, detected in real-time with LightCycler hybridisation probes, was related to the indexes of insulin sensitivity. Furthermore, the possible role of this variant on insulin secretion was studied by means of insulin release indexes derived from oral tolerance test (OGTT). Twenty-four point five percent (24.5%) (no.=15) of the obese subjects proved to be carriers of the G972R variant. M index (p<0.05), non-oxidative glucose (p<0.01), insulin clearance (p<0.03) and insulin sensitivity index (ISI) (p<0.005) were all significantly reduced in G972R carriers compared to non-carriers, indicating a significant reduction in insulin sensitivity in carriers of the variant. A logistic regression analysis confirmed the independent association between the G972R variant and reduced insulin sensitivity (p<0.03). The interaction between obesity and the G972R variant was also independently associated with a reduced insulin sensitivity (p<0.005), suggesting that obesity and G972R variant were more than additive in predicting insulin resistance. The analysis of insulin release indexes did not show any significant differences. Our results demonstrate the association of the G972R variant of the IRS-1 gene with reduced insulin sensitivity in obese subjects, and indicate a possible interaction between the IRS-1 variant and obesity in worsening of insulin sensitivity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0391-4097
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
754-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15636429-Adult, pubmed-meshheading:15636429-Female, pubmed-meshheading:15636429-Gene Frequency, pubmed-meshheading:15636429-Glucose Clamp Technique, pubmed-meshheading:15636429-Glucose Tolerance Test, pubmed-meshheading:15636429-Humans, pubmed-meshheading:15636429-Hyperinsulinism, pubmed-meshheading:15636429-Hypoglycemic Agents, pubmed-meshheading:15636429-In Situ Hybridization, Fluorescence, pubmed-meshheading:15636429-Insulin, pubmed-meshheading:15636429-Insulin Receptor Substrate Proteins, pubmed-meshheading:15636429-Insulin Resistance, pubmed-meshheading:15636429-Logistic Models, pubmed-meshheading:15636429-Male, pubmed-meshheading:15636429-Mutation, pubmed-meshheading:15636429-Obesity, pubmed-meshheading:15636429-Phosphoproteins, pubmed-meshheading:15636429-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15636429-Spectrometry, Fluorescence
pubmed:year
2004
pubmed:articleTitle
The G972R variant of the insulin receptor substrate-1 (IRS-1) gene is associated with insulin resistance in "uncomplicated" obese subjects evaluated by hyperinsulinemic-euglycemic clamp.
pubmed:affiliation
Department of Clinical Sciences, Division of Endocrinology, University of Rome "La Sapienza", Rome, Italy. marco.baroni@uniroma1.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't