Poster Topical Area: Obesity
Location: Hall D
Poster Board Number: 735
Objectives: A common single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (Oprm1 A118G) results in a functional amino acid substitution (N40D) at a putative N-glycosylation site. The A118G variant is estimated to have a global allele frequency of 10%, as high as 60% in individuals of Asian descent, and incurs a predisposition to alcohol and drug abuse, as well as altered nociception and analgesia efficacy. In addition, the GG variant has been associated with Binge eating Disorder (BED) in an obese population. The primary objective of our study was to determine whether the A118G polymorphism influences binge-like eating in mice.
Methods: Transgenic mice with an equivalent substitution in Exon 1 (A112G) were exposed to an established rodent model of dietary-induced binge eating. Six-week-old homozygous AA/GG male mice randomized to one of four feeding schedules, including Restrict-Binge, Binge, Restrict, and Naive groups (n=8/group), were provided with intermittent access (30 min) to a highly palatable "binge" food (vegetable shortening plus 10% sucrose) twice weekly, with or without food restriction (24-hours prior) for 12 binges. Following 12 binges, male AA/GG mice underwent 2-Bottle Preference Testing using Intralipid lipid emulsion (2.5%, 5%, 10%).
Results: For 30 min feeding access, there was a significant genotype x group effect [(F(3, 51) = 3.1, p < 0.05). For lipid preference, there was significant concentration effect and a group effect [F(3, 32) = 2.8, p=.05]. A planned comparisons revealed lower fat preference in Restrict (p< 0.01) and Restrict-Binge (p < 0.05) compared to Naïve males.
Conclusion: Our emerging results indicate that the A118G mouse equivalent polymorphism influences binge eating-related outcomes. In addition, 2-bottle preference scores in male mice suggest that a dietary history of intermittent restriction reduces lipid preference.
Princeton, New Jersey