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Lee, K.W.* ; Abrahamowicz, M.* ; Leonard, G.T.* ; Richer, L.* ; Perron, M.* ; Veillette, S.* ; Reischl, E. ; Bouchard, L.* ; Gaudet, D.* ; Paus, T.* ; Pausova, Z.*

Prenatal exposure to cigarette smoke interacts with OPRM1 to modulate dietary preference for fat.

J. Psychiatry Neurosci. 39, 38-45:130263 (2015)
Verlagsversion DOI PMC
Free by publisher
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
BACKGROUND: Preference for fatty foods is a risk factor for obesity. It is a complex behaviour that involves the brain reward system and is regulated by genetic and environmental factors, such as the opioid receptor mu-1 gene (OPRM1) and prenatal exposure to maternal cigarette smoking (PEMCS). We examined whether OPRM1 and PEMCS interact in influencing fat intake and whether exposure-associated epigenetic modifications of OPRM1 may mediate this gene-environment interaction. METHODS: We studied adolescents from a French Canadian genetic founder population, half of whom were exposed prenatally to maternal cigarette smoking. Fat intake was assessed with a 24-hour food recall in the form of a structured interview conducted by a trained nutritionist. The OPRM1 variant rs2281617 was genotyped for the whole sample with the Illumina Human610-Quad and HumanOmniExpress BeadChips. Methylation of blood DNA was assessed at 21 CpGs across OPRM1 in a subset of the sample using the Illumina HumanMethylation450 BeadChip. RESULTS: We included 956 adolescents in our study. In the whole sample, OPRM1 (T carrier in rs2281617) was associated with lower fat intake (-1.6%, p = 0.017), and PEMCS was associated with higher fat intake (+1.6%, p = 0.005). OPRM1 and PEMCS interacted with each other (p = 0.003); the "protective" (fat intake-lowering) allele of OPRM1 was associated with lower fat intake in nonexposed (-3.2%, p < 0.001) but not in exposed individuals (+0.8%, p = 0.42). Further, PEMCS was associated with lower DNA methylation across multiple CpGs across OPRM1 in exposed versus nonexposed individuals (p = 0.031). LIMITATIONS: A limitation of our study was its cross-sectional design. CONCLUSION: Our study suggests that PEMCS may interact with OPRM1 in increasing fat preference. Silencing of the protective OPRM1 allele in exposed adolescents might be related to epigenetic modification of this gene.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Differential Dna Methylation; Maternal Smoking; Weight Change; Obesity; Gene; Genome; Adolescence; Pregnancy; Food; Variants
ISSN (print) / ISBN 1180-4882
e-ISSN 1488-2434
Zeitschrift Journal of Psychiatry & Neuroscience : An International Journal
Quellenangaben Band: 39, Heft: 4, Seiten: 38-45, Artikelnummer: 130263 Supplement: ,
Verlag Canadian Medical Assoc.
Verlagsort Ottawa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Epidemiology II (EPI2)