Abstract
Animal research finds that insulin regulates dopamine signaling and reward behavior, but similar research in humans is lacking. We investigated whether individual differences in body mass index, percent body fat, pancreatic β-cell function, and dopamine D2 receptor binding were related to reward discounting in obese and non-obese adult men and women. Obese (n = 27; body mass index>30) and non-obese (n = 20; body mass index<30) adults were assessed for percent body fat with dual-energy X-ray absorptiometry and for β-cell function using disposition index. Choice of larger, but delayed or less certain, monetary rewards relative to immediate, certain smaller monetary rewards was measured using delayed and probabilistic reward discounting tasks. Positron emission tomography using a non-displaceable D2-specific radioligand, [11C](N-methyl)benperidol quantified striatal D2 receptor binding. Groups differed in body mass index, percent body fat, and disposition index, but not in striatal D2 receptor specific binding or reward discounting. Higher percent body fat in non-obese women related to preference for a smaller, certain reward over a larger, less likely one (greater probabilistic discounting). Lower β-cell function in the total sample and lower insulin sensitivity in obese related to stronger preference for an immediate and smaller monetary reward over delayed receipt of a larger one (greater delay discounting). In obese adults, higher striatal D2 receptor binding related to greater delay discounting. Interestingly, striatal D2 receptor binding was not significantly related to body mass index, percent body fat, or β-cell function in either group. Our findings indicate that individual differences in percent body fat, β-cell function, and striatal D2 receptor binding may each contribute to altered reward discounting behavior in non-obese and obese individuals. These results raise interesting questions about whether and how striatal D2 receptor binding and metabolic factors, including β-cell function, interact to affect reward discounting in humans.
Highlights
Human obesity is associated with altered dopamine (DA) function [1], altered DA D2-like receptor binding in brain reward regions [2,3], altered reward-related behavior [4,5,6], and insulin dysregulation [7,8]
The current study provides preliminary evidence of relationships between reward discounting behavior and 3 biological constructs related to obesity: percent body fat (PBF), pancreatic β-cell function, and striatal DA D2 receptor (D2R) binding in non-obese and obese humans
This is the first human study of the relations between pancreatic insulin secretion and any type of discounting reward behavior in individuals carefully screened for prediabetes and diabetes
Summary
Human obesity is associated with altered dopamine (DA) function [1], altered DA D2-like receptor binding in brain reward regions [2,3], altered reward-related behavior [4,5,6], and insulin dysregulation [7,8]. How these factors relate to each other remains unclear. In insulin-resistant individuals, the increased rate of brain glucose metabolism normally associated with insulin infusion is decreased, in regions related to reward such as ventral striatum [23]. There are no published human studies of the relations among pancreatic β-cell insulin secretion, striatal D2 receptor (D2R) binding, and food or non-food reward discounting behavior in the same individual
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