| Genetic variance in the consumption of sweet and bitter tastants as well as fat intake has been established through the use of inbred mouse strains. The use of limited ranges of strains, limited sets of concentrations, a failure to examine genetic variance for glucoprivic- or lipoprivic-induced intake formed the basis of this dissertation. The aims investigated whether 11 inbred (A/J, AKR/J, BALB/c/J, CBA/J, C3H/He/J, C57BL/6/J, C57BL/10/J, DBA/2/J, SWR/J and 129P3/J) and one outbred (CD-1) mouse strains differed in their intake of a wide concentration range of sucrose (0.0001-20%) or fat (Intralipid: 0.00001-5%) and intake (1-4 h) following the anti-metabolic glucose analogue, 2-deoxy-D-glucose (2DG: 200-800 mg/kg) or the free fatty acid oxidation inhibitor, mercaptoacetate (MA: 5-100 mg/kg).;Sucrose intake was assessed across 9 concentrations using two-bottle tests controlling for concentration order, bottle positions, and kilocalorie intake consumed as sucrose. Strain specific differences were observed for the amounts and percentages of sucrose intake as well as for compensatory decreases in chow intake as sucrose concentrations increased. Sucrose intake correlated with previous data for saccharin intake and variants of the Tas1r3 taste receptor gene, particularly at lower concentrations.;To assess whether strain differences in fat intake were similar to those of sucrose intake, a highly similar methodology examined intake of Intralipid across 9 concentrations in the same strains. There were also clear and consistent strain differences across a wide range of measures for Intralipid intake. Interestingly, there were marked positive correlations in strain-specific intakes of sucrose and Intralipid.;Glucoprivic intakes were evaluated following systemic 2DG. Strain specific differences were observed in 2DG-induced feeding across different doses. A parallel study evaluating strain-specific lipoprivic intake used MA. Strain specific differences were also observed in MA-induced feeding. Correlations were generally not observed between lipoprivation and glucoprivation, lipoprivation and fat intake, and glucoprivation and sucrose intake, suggesting different mechanisms of action for observed genetic variance.;Together, the results of the four aims for this dissertation demonstrate a strong and distinct role for genetic variance in these four types of homeostatic ingestive responses that have implications for elucidating the genetic and environmental factors that may contribute to obesity. |
