Abstract
Background
Excessive gestational weight gain is associated with postpartum weight retention and downstream child obesity. Dopamine plays a critical role in the regulation of energy intake and body weight. The purpose of this study was to examine the relationship between excessive gestational weight gain and dopamine pathway-related polymorphisms, namely the variable nucleotide tandem repeat in the 3′untranslated region (UTR) region of the SLC6A3 (DAT-1) dopamine transporter gene and the 30-base pair variable nucleotide tandem repeat polymorphism of the 5′UTR of the monoamine oxidase-A (MAO-A) gene.
Methods
Ninety-three women of mean age 31.7 ± 4.2 years were recruited from the Ottawa and Kingston birth cohort and assessed at 12–20 weeks’ gestation. Mean body mass index was 22.7 ± 2.5 kg/m2. Excessive gestational weight gain was defined according to the 2009 Institute of Medicine guidelines based on body mass index. Genotype analyses were performed using polymerase chain reaction and agarose gel electrophoresis.
Results
There was no relationship between the prevalence or magnitude of excessive gestational weight gain among women with the 3′ UTR single nucleotide polymorphism of the DAT-1 gene. However, 70% (19 of 27) of women carrying the MAO-A 4/4 (high activity) allele exceeded recommendations for gestational weight gain compared with 48% (32 of 60) of those with the pooled 3/3, 3/4, and 3/3.5 (low activity) alleles (P < 0.05). Similarly, those with the MAO-A 4/4 allele had significantly greater gestational weight gain than those with the 3/3, 3/4, or 3/3.5 pooled genotypes (19.3 ± 4.1 versus 17.0 ± 5.0 kg, P = 0.03).
Conclusion
Carriers of the 4/4 variants of the MAO-A gene may be at increased risk for excessive gestational weight gain.
Acknowledgments
The authors would like to thank all the subjects who participated in the study and all the research staff who assisted with data collection. We would also like to thank Nancy Carson and Barron Gin from the Apoptosis Research Center at the Children’s Hospital of Eastern Ontario for providing us with laboratory space and equipment and for overseeing the genotyping process. At the time the study was conducted, GSG, MW, and ED were supported by new investigator awards from the Canadian Institutes of Health Research. JDC was supported by a University of Ottawa graduate scholarship. ZMF was supported by an Ontario Graduate Scholarship. KBA and GG held a Canadian Foundation of Innovation Award to equip the laboratory at the Children’s Hospital of Eastern Ontario Research Institute where the study was conducted.
Disclosure
The authors report no conflicts of interest in this work.