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Are dopamine-related genotypes risk factors for excessive gestational weight gain?

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...

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Autores principales: Goldfield, Gary S, Dowler, Lauren Marie, Walker, Mark, Cameron, Jameason D, Ferraro, Zachary M, Doucet, Eric, Adamo, Kristi B
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665497/
https://www.ncbi.nlm.nih.gov/pubmed/23723720
http://dx.doi.org/10.2147/IJWH.S43935
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author Goldfield, Gary S
Dowler, Lauren Marie
Walker, Mark
Cameron, Jameason D
Ferraro, Zachary M
Doucet, Eric
Adamo, Kristi B
author_facet Goldfield, Gary S
Dowler, Lauren Marie
Walker, Mark
Cameron, Jameason D
Ferraro, Zachary M
Doucet, Eric
Adamo, Kristi B
author_sort Goldfield, Gary S
collection PubMed
description 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/m(2). 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.
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spelling pubmed-36654972013-05-30 Are dopamine-related genotypes risk factors for excessive gestational weight gain? Goldfield, Gary S Dowler, Lauren Marie Walker, Mark Cameron, Jameason D Ferraro, Zachary M Doucet, Eric Adamo, Kristi B Int J Womens Health Original Research 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/m(2). 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. Dove Medical Press 2013-05-20 /pmc/articles/PMC3665497/ /pubmed/23723720 http://dx.doi.org/10.2147/IJWH.S43935 Text en © 2013 Goldfield et al, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
spellingShingle Original Research
Goldfield, Gary S
Dowler, Lauren Marie
Walker, Mark
Cameron, Jameason D
Ferraro, Zachary M
Doucet, Eric
Adamo, Kristi B
Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title_full Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title_fullStr Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title_full_unstemmed Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title_short Are dopamine-related genotypes risk factors for excessive gestational weight gain?
title_sort are dopamine-related genotypes risk factors for excessive gestational weight gain?
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665497/
https://www.ncbi.nlm.nih.gov/pubmed/23723720
http://dx.doi.org/10.2147/IJWH.S43935
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