HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) All Versions of this Article: db06-0506v1 56/5/1198    most recent Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Menzaghi, C. Articles by Doria, A. Search for Related Content PubMed PubMed Citation Articles by Menzaghi, C. Articles by Doria, A. Social Bookmarking                What's this?

Genetic Influences of Adiponectin on Insulin Resistance, Type 2 Diabetes, and Cardiovascular Disease.

¹Research Unit of Diabetology and Endocrinology, Scientific Institute "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy
²Department of Clinical Sciences, University La Sapienza, Rome, Italy
³Research Division, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, MA

Correspondence: alessandro.doria{at}joslin.harvard.edu

Recent evidence points to molecules secreted by the adipose tissue, or adipokines, as possible links between increased adipose mass and metabolic abnormalities. Among these molecules, adiponectin has drawn much attention because of its insulin sensitizing and antiatherogenic actions, suggesting that genetic deficits in its production or action may contribute to insulin-resistance and coronary artery disease (CAD). A meta-analysis of the data published to date supports this hypothesis. Two independent effects, corresponding to the two linkage disequilibrium blocks that can be identified at the adiponectin locus, appear to be present. In the 5' block, the g.-11391G>A variant has a modest but significant effect on adiponectinemia, with a mean difference between genotypes of 1.64 ng/ml (95% CI=0.88-2.41, p=0.01). In the 3' block, the g.+276G>T variant is a strong determinant of insulin-resistance and CAD, with minor allele homozygotes having lower HOMA_IR index (-0.36 units, 95% CI=0.24-0.47, p<0.0001) and cardiovascular risk (OR=0.55, 95%CI 0.38-0.80) than carriers of other genotypes. No consistent effect on BMI or risk of type 2 diabetes is evident. Polymorphisms in the genes coding for the adiponectin receptors may also influence the risk of insulin-resistance and CAD, but data on these genes are still too sparse to draw firm conclusions. In summary, the studies published to date indicate that polymorphisms at the adiponectin locus are indeed predictors of circulating adiponectin levels, insulin-sensitivity, and atherosclerosis, highlighting the pivotal role of this adipokine in the modulation of metabolism and atherogenesis.

CiteULike

Del.icio.us

Digg

Reddit

Technorati