| D2 Thr92Ala and PPARγ2 Pro12Ala Polymorphisms Interact in the Modulation of Insulin Resistance in Type 2 Diabetic Patients. | |
| | |
MedLine Citation:
|
PMID: 20930717 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
|
Type 2 deiodinase (D2) converts T4 into its active metabolite T3, an essential step in thyroid metabolism. A Thr92Ala polymorphism in the gene encoding D2 has been inconsistently associated with insulin resistance (IR). Recently, it was reported that the D2 Thr92Ala (rs225014) and the peroxisome proliferator-activated receptor (PPAR) γ2 Pro12Ala (rs1801282) polymorphisms interact in the modulation of metabolic syndrome in nondiabetic subjects. Here, we investigated the effect of both polymorphisms, isolated or in combination, on IR in patients with type 2 diabetes mellitus (DM2). The D2 Thr92Ala and PPARγ2 Pro12Ala polymorphisms were genotyped in 721 DM2 patients. IR was evaluated using the homeostasis model assessment-IR (HOMA(IR)) index in a subgroup of 246 DM2 subjects. The frequencies of D2 Ala92 and PPARγ2 Ala12 variants were 0.390 and 0.074, respectively. Patients carrying D2 Ala/Ala genotype had a higher fasting plasma insulin and HOMA(IR) index as compared to patients carrying Thr/Ala or Thr/Thr genotypes (P = 0.022 and P = 0.001, respectively). A significant synergistic effect was observed between D2 Thr92Ala and PPARγ2 Pro12Ala polymorphisms on HOMA(IR) index, with carriers of both D2 Ala/Ala genotype and PPARγ2 Ala12 allele showing the highest HOMA(IR) values, after adjusting for age, gender, BMI, and use of medication for DM2 (P = 0.010). In conclusion, DM2 patients harboring both D2 Ala/Ala genotype and PPARγ2 Ala12 allele seem to present more severe IR than those with other D2/PPARγ2 genotype combinations. These findings suggest that these polymorphisms interact in the IR modulation, which may constitute a potential therapeutic target. |
| | |
Authors:
|
Aline A F Estivalet; Leonardo B Leiria; José M Dora; Jakeline Rheinheimer; Ana P Bouças; Ana L Maia; Daisy Crispim |
Related Documents
:
|
20966027 - Insulin resistance and necroinflammation drives ductular reaction and epithelial-mesenc... 18556967 - Resting energy expenditure in insulin resistance falls with decompensation of insulin s... 15107927 - Comparison of the homeostasis model assessment and quantitative insulin sensitivity che... 10652907 - Hypertension, insulin resistance and atherosclerosis. 1978827 - Multigenic basis for type i diabetes. association of hras1 polymorphism with hla-dr3, d... 1605837 - The possible mechanism of binding interaction of insulin molecule with its receptor. |
Publication Detail:
|
Type: Journal Article Date: 2010-10-07 |
Journal Detail:
|
Title: Obesity (Silver Spring, Md.) Volume: 19 ISSN: 1930-7381 ISO Abbreviation: Obesity (Silver Spring) Publication Date: 2011 Apr |
Date Detail:
|
Created Date: 2011-03-28 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101264860 Medline TA: Obesity (Silver Spring) Country: United States |
Other Details:
|
Languages: eng Pagination: 825-32 Citation Subset: IM |
Affiliation:
|
Endocrine Division, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul, Rio Grande do Sul, Brazil. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Lifestyle and Socioeconomic-Status Modify the Effects of ADRB2 and NOS3 on Adiposity in European-Ame...
Next Document: Identifying patterns of eating and physical activity in children: a latent class analysis of obesity...