Food intake and obesity related phenotypes are greatly affected by economic factors and yet very little is known about the interaction of economic factors, genetics, behavior, and obesity phenotypes. Recent human population research suggests that a decreasing price of high fat food relative to low fat food has contributed to the current obesity epidemic in humans. The two key elements in this argument are choice and costs. We incorporate these key elements in a closed economy mouse model to study the interactions of economics, genetics, and obesity related phenotypes, using normal mice, and mice with a mutation in the hypothalamus-expressed Tub gene, which has a phenotype of adult onset obesity. Results for both genotypes indicate that as the price of the high fat food falls, consumption of that food increases and consumption of the low fat food declines, but not enough to offset the increase in high fat food so total intake and weight increases, with no statistically-significant differences between genotypes. These results are in contrast to previous literature based on an ad lib, no choice food setting. In addition, in our closed economy model, the Tub mutant showed a numerical and statistically significant increase in body fat percentage and glucose intolerance, whereas these increases were only numerical for the normal mice. Both genotypes showed numerical but statistically insignificant increases in leptin and ghrelin levels. These results show that accounting for choice in neuroeconomic studies is important to understanding the complex regulation of intake, body weight and other related phenotypes.
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