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Increased Abdominal Obesity in Subjects with a Mutation in the 5‐HT 2A Receptor Gene Promoter
Author(s) -
ROSMOND ROLAND,
BOUCHARD CLAUDE,
BJÖRNTORP PER
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04319.x
Subject(s) - endocrinology , medicine , leptin , abdominal obesity , genotype , ghrelin , allele , obesity , insulin , biology , insulin resistance , glucocorticoid receptor , hormone , gene , waist , glucocorticoid , genetics
A bstract : In the present study, we examined the potential impact of the 5‐HT 2A −1438G/A promoter polymorphism on obesity and estimates of insulin, glucose, and lipid metabolism as well as circulating hormones, including salivary cortisol, in 284 unrelated Swedish men born in 1944. The subjects were genotyped by using PCR amplification of the promoter region of the gene for 5‐HT 2A followed by digestion with the restriction enzyme Msp I. The frequencies were 0.39 for allele −1438A and 0.61 for allele −1438G. Homozygotes for the −1438G allele had, in comparison with −1438A/A subjects, higher body mass index (BMI), waist‐to‐hip ratio (WHR), and abdominal sagittal diameter. Moreover, cortisol escape from 0.25 mg dexamethasone suppression was found in subjects with the −1438A/G genotype. Serum leptin, fasting insulin and glucose, as well as serum lipids were not different across the −1438G/A genotype groups. From these results, we suggest the possibility that an abnormal production rate of the 5‐HT 2A gene product might lead to the development of abdominal obesity. The pathophysiology could involve stress factors that destabilize the serotonin‐hypothalamic‐pituitary‐adrenal systems in those with genetic vulnerability in the serotonin receptor gene.