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

ABSTRACT:

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

SUBMITTER: Lee KW 

PROVIDER: S-EPMC4275330 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature