Journal Name:
Metabol. Clin.Exper.
Article Title:
Adiponectin levels are reduced, independent of polymorphisms in the adiponectin gene, after supplementation with α-linolenic acid among healthy adults
Date Written:
2007
Volume:
56
Number:
0
Page:
1209
Author(s):
Nelson, T.L.; Stevens, J.R.; Hickey, M.S.
Article:
Adiponectin is an adipocyte-derived peptide that is inversely associated with the plasma inflammatory biomarkers C-reactive protein and tumor necrosis factor α, as well as obesity, insulin resistance, and heart disease. Variation in the gene that produces adiponectin is associated with obesity, insulin resistance, and adiponectin levels. Specifically, the single nucleotide polymorphisms (SNPs) G276T (intron 2) and T45G (exon 2) have been associated with varying levels of adiponectin, risk of type 2 diabetes mellitus as well as body mass index (BMI), fasting insulin, and glucose. α-linolenic acid (ALA, 18:3 n-3) can lower proinflammatory markers such as C-reactive protein and may be associated with increasing insulin sensitivity . The purpose of this study was to determine if an isoenergetic diet supplemented with 5% of energy from ALA, alters adiponectin levels or estimates of insulin sensitivity. Additionally variations in SNP 276 or 45 of the adiponectin gene were assessed.
The first objective was to determine whether an isocaloric intervention using ALA would alter adiponectin levels among overweight, otherwise healthy, males and females, and the second aim was to test for any potential modification of this intervention by 2 single nucleotide polymorphisms (276 and 45) in the adiponectin gene. Subjects included healthy adult males and females (∼81% female; average age, 38 years) with increased waist circumference (mean, 99 cm) and body mass index (mean, 30 kg/m2) who were free of chronic disease, not taking medications, and sedentary. Subjects met weekly with a registered dietician for 8 weeks. The control subjects (n = 27) were instructed not to alter their habitual diet and the ALA group (n = 30) was instructed to follow an enriched ALA diet by using flaxseed oil capsules (increasing ALA to 5% of total energy intake) and to lower their dietary fat consumption by a commensurate amount.
Significant decreases (P = .02) in adiponectin (10.12 μg/mL pre, 9.23 μg/mL post) in the ALA group as compared with the control group (7.93 μg/mL pre, 8.10 μg/mL post) after the intervention were found. A decline in adiponectin in all genotype groups was noted with the greatest decline among those carrying the rare T allele of single nucleotide polymorphism 276. There were no significant changes in fasting insulin, glucose, or quantitative insulin sensitivity check index values as a result of this intervention.
The clinical significance of the small decrease in adiponectin (0.89 μg/mL) among the intervention group is not clear because no changes in insulin, glucose, or insulin sensitivity were found after ALA supplementation. Importantly, however, this small decrease could have clinical relevance in relation to overall cardiovascular disease risk as previous studies have shown that adiponectin was significantly lower in diabetic patients with coronary artery disease (CAD) vs those without CAD and that these differences were quite small: 1.3 μg/mL. Considering that our study was primarily among women (80%), with an average age of 38 years who were free of diabetes, known heart disease, or other inflammatory condition including asthma or arthritis, a decrease of 0.89 μg/mL may pose a significant risk for cardiovascular outcomes if these subjects continued with this ω-3 fatty acid supplement into their fifties. Future studies will be needed to further ascertain the long-term effects of ω-3 fatty acid supplementation on adiponectin levels.
Regarding the genetic modification of this dietary intervention, a decrease in adiponectin among those carrying the rare T allele of SNP 276 and the rare G allele of SNP 45 was reported, with the greatest changes among those carrying the T allele of SNP 276 (13% vs 9%). Most of the previous work has considered the adiponectin gene in relation to metabolic syndrome variables (eg, insulin, glucose, diabetes status, BMI, etc) without considering the response to a dietary intervention.
In conclusion, this study suggests that supplementing with ALA for 8 weeks may lower adiponectin levels among healthy individuals, and this effect appears to be independent of polymorphisms in the adiponectin gene. Although the change in adiponectin in response to the ω-3 fatty acids was not accompanied by any change in glucose, insulin, or quantitative insulin sensitivity check index, long-term implications of such a decrease should be considered in future studies.
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