Prenatal exposure to cigarette smoke interacts with <i>OPRM1</i> to modulate dietary preference for fat

Lee, Ken W. K.; Abrahamowicz, Michał; Leonard, Gabriel; Richer, Louis; Perron, Michel; Veillette, Suzanne; Reischl, Eva; Bouchard, Luigi; Gaudet, Daniel; Paus, Tomáš; Pausová, Zdenka

doi:10.1503/jpn.130263

Cited by 20 publications

(15 citation statements)

References 48 publications

(73 reference statements)

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“…Among 956 adolescents, the T allele in OPRM1 was associated with lower fat intake but only in those without prenatal exposure to cigarette smoke [72]. DNA methylation was significantly reduced within several CpGs across OPRM1 among adolescents exposed to prenatal maternal cigarette smoking compared with those not exposed [72].…”

Section: Obesity-predisposing Gene Variants Interact With Non-modifiamentioning

confidence: 92%

“…Prenatal exposure to maternal cigarette smoking was found to interact with genetic variation in OPRM1 to modulate fat intake in offspring [72]. Among 956 adolescents, the T allele in OPRM1 was associated with lower fat intake but only in those without prenatal exposure to cigarette smoke [72].…”

Section: Obesity-predisposing Gene Variants Interact With Non-modifiamentioning

confidence: 98%

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The importance of gene–environment interactions in human obesity

2016

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The worldwide obesity epidemic has been mainly attributed to lifestyle changes. However, who becomes obese in an obesity-prone environment is largely determined by genetic factors. In the last 20 years, important progress has been made in the elucidation of the genetic architecture of obesity. In parallel with successful gene identifications, the number of gene-environment interaction (GEI) studies has grown rapidly. This paper reviews the growing body of evidence supporting gene-environment interactions in the field of obesity. Heritability, monogenic and polygenic obesity studies provide converging evidence that obesity-predisposing genes interact with a variety of environmental, lifestyle and treatment exposures. However, some skepticism remains regarding the validity of these studies based on several issues, which include statistical modelling, confounding, low replication rate, underpowered analyses, biological assumptions and measurement precision. What follows in this review includes (1) an introduction to the study of GEI, (2) the evidence of GEI in the field of obesity, (3) an outline of the biological mechanisms that may explain these interaction effects, (4) methodological challenges associated with GEI studies and potential solutions, and (5) future directions of GEI research. Thus far, this growing body of evidence has provided a deeper understanding of GEI influencing obesity and may have tremendous applications in the emerging field of personalized medicine and individualized lifestyle recommendations.

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Section: Obesity-predisposing Gene Variants Interact With Non-modifiamentioning

confidence: 92%

Section: Obesity-predisposing Gene Variants Interact With Non-modifiamentioning

confidence: 98%

The importance of gene–environment interactions in human obesity

2016

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“…Additionally, intrauterine exposure to cigarette smoke may affect the activity of the opioid receptor mu-1 through an epigenetic mechanism. Methylation of this gene is associated with increased fat consumption in prenatally exposed adolescents [34**]. …”

Section: Adverse Health Outcomesmentioning

confidence: 99%

Tobacco, e-cigarettes, and child health

Peterson

Hecht

2017

Current Opinion in Pediatrics

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Purpose of the review The availability of the Children’s Health Exposure Assessment Resource funded by the National Institute of Environmental Health Sciences provides new opportunities for exploring the role of tobacco smoke exposure in causing harm to children. Findings Children of smokers are exposed to nicotine and other harmful tobacco smoke chemicals in utero as well as in their environment. This passive exposure to tobacco smoke has a variety of negative effects on children. In utero exposure to tobacco smoke causes poor birth outcomes and influences lung, cardiovascular and brain development, placing children at increased risk of a number of adverse health outcomes later in life such as obesity, behavioral problems and cardiovascular disease. Furthermore, most smokers start in their adolescence, an age of increased nicotine addiction risk. Biomarkers of tobacco exposure helps clarify the role tobacco chemicals play in influencing health both in childhood and beyond. While e-cigarettes appear to be a nicotine delivery device of reduced harm, it appears to be a gateway to the use of combustible cigarette smoking in adolescents. Summary Pediatric researchers interested in elucidating the role of tobacco smoke exposure in adverse outcomes in children should incorporate biomarkers of tobacco exposure in their studies.

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“…In a genome-wide association study, we also showed that dietary preference for fat (as well as body adiposity) is associated with genetic variation in the opioid receptor mu 1 gene (OPRM1) (Haghighi et al, 2014). Finally, we have demonstrated that MSP is associated with modifications of DNA methylation that persist into adolescence of the exposed offspring (Lee et al, 2014a), and that some of these modifications are present in OPRM1, and may inhibit expression of the protective (fat intake-lowering) allele of this gene (Lee et al, 2014b). Taken together, these observations suggest (a) the presence of relationships between the brain-reward system, dietary preference for fat and obesity; (b) perturbations of these relationships by MSP and genetic variations in OPRM1; and (c) DNA methylation as a possible molecular mechanism underlying interactions between environment (MSP) and genes (OPRM1).…”

Section: Saguenay Youth Study: Highlightsmentioning

confidence: 86%

Saguenay Youth Study: A multi-generational approach to studying virtual trajectories of the brain and cardio-metabolic health

Paus

Pausová

Abrahamowicz

et al. 2015

Developmental Cognitive Neuroscience

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This paper provides an overview of the Saguenay Youth Study (SYS) and its parental arm. The overarching goal of this effort is to develop trans-generational models of developmental cascades contributing to the emergence of common chronic disorders, such as depression, addictions, dementia and cardio-metabolic diseases. Over the past 10 years, we have acquired detailed brain and cardio-metabolic phenotypes, and genome-wide genotypes, in 1029 adolescents recruited in a population with a known genetic founder effect. At present, we are extending this dataset to acquire comparable phenotypes and genotypes in the biological parents of these individuals. After providing conceptual background for this work (transactions across time, systems and organs), we describe briefly the tools employed in the adolescent arm of this cohort and highlight some of the initial accomplishments. We then outline in detail the phenotyping protocol used to acquire comparable data in the parents.

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

Cited by 20 publications

References 48 publications

The importance of gene–environment interactions in human obesity

The importance of gene–environment interactions in human obesity

Tobacco, e-cigarettes, and child health

Saguenay Youth Study: A multi-generational approach to studying virtual trajectories of the brain and cardio-metabolic health

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