Additive, nonadditive and maternal genetic effects on adiposity in mice fed different levels of fat

Polygenic obese (M16), nonobese (ICR) and reciprocal crossbred (M16 male x ICR female and ICR male x M16 female) mice were fed ad libitum diets containing 1, 5 or 25% fat from 3 to 10 weeks of age. Epididymal and subcutaneous fat depot weights (E, S) and depot weights as a proportion of empty body weight (E%, S%) were used as measures of adiposity at 6 and 10 weeks of age. Genetic differences in adiposity among the four populations were partitioned into average direct (a), average maternal (m) and direct heterotic (h) effects. Line M16 was greater than ICR at both 6 and 10 weeks in E (81% at 6 weeks and 114% at 10 weeks), S (82%, 73%), E% (27%, 37%) and S% (26%, 12%). Average direct genetic effects, as determined by a, accounted for 60% of the M16 vs. ICR line difference in E and S at six weeks, the remainder of the difference being due to m. The major portion of the line difference in E% and S% at 6 weeks was accounted for by m. At ten weeks of age, most of the line difference in E, S, E% and S% was due to additive direct genetic effects while the contribution of maternal genetic effects was negligible. Heterosis was sizeable for all measures of adiposity, varying from 10.8% in S% at 10 weeks to 26.8% in E at six weeks, possibly indicating the presence of directional dominance. E and E% increased significantly with the increase in dietary fat percent, but S and S% were not affected. Interactions of genotype with level of dietary fat percent were not significant for the epididymal or subcutaneous fat depot weights or proportional weights.