A study of possible associations between single nucleotide polymorphisms in the serotonin receptor 1A, 1B, and 2C genes and self-reported ejaculation latency time.

Patrik Jern, L Westberg, A Johansson, A Gunst, E Eriksson, Kenneth Sandnabba, Pekka Santtila

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Sammanfattning

INTRODUCTION Previous research has indicated that serotonergic genes may influence ejaculatory function. Attempts to investigate effects of polymorphisms in serotonergic genes have been carried out, but so far, no study has conducted exploratory genotype analyses regarding the serotonin receptor 1A, 1B, and 2C subtypes, which have been hypothesized to mediate the inhibitory effects of serotonin on ejaculation in rodents. AIM The aim of the present study was to investigate effects of a total of six single nucleotide polymorphisms (SNPs) located in genes encoding serotonin receptor subtypes 1A, 1B, and 2C on self-reported ejaculation latency time. METHODS A retrospective self-report measure of ejaculation latency time was used to investigate ejaculatory function in a population-based sample of 1,399 male twins. DNA was collected using self-administered saliva sampling. MAIN OUTCOME MEASURE Calculations of allelic effects were conducted using the Generalized Estimating Equations module of PASW 18.0, which appropriately controls for between-subjects dependence.\nRESULTS\nOut of six investigated polymorphisms, two SNPs (both serotonin receptor 5-HT(1B) linked) had a significant main effect on ejaculation latency time. Of these, one (rs11568817) remained significant after Bonferroni correction for multiple testing, indicating that individuals homozygous for the G allele had significantly shorter ejaculation latencies. CONCLUSIONS The results of this study support the hypothesis that serotonergic genes play a role in ejaculatory function in the general population. Replication of the results of the present study is warranted.
OriginalspråkOdefinierat/okänt
Sidor (från-till)866–872
TidskriftThe Journal of Sexual Medicine
Volym9
Utgåva3
DOI
StatusPublicerad - 2012
MoE-publikationstypA1 Tidskriftsartikel-refererad

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