۱- Introduction

۲- Materials and methods

۳- Results

۴- Discussion

References

Abstract

Although hormonal and metabolic factors are well known to influence obesity, recent evidence suggests that obesity may be influenced also by changes in reward sensitivity akin to that seen in other ‘reward pathologies’, like substance use disorders. The current study sought to isolate changes in reward that may occur after the onset of diet-induced obesity by characterizing the economic demand for caloric (sucrose) and non-caloric (saccharin) reinforcers in a preclinical model of diet-induced obesity (DIO). We utilized economic demand analysis to measure baseline demand intensity (Q0) and demand elasticity (α) for sucrose and saccharin reinforcers in rats. After baseline measures were collected, rats were assigned randomly to a high-fat (HF) diet or low-fat (LF) control diet. After 8-weeks of diet exposure, HF rats were divided into obesity-resistant (OR) or obesity-prone (OP) groups based on weight after the 8-week HF diet exposure. Post-DIO demand data for each reinforcer were reassessed. At baseline, rats had higher demand intensity and lower elasticity for sucrose compared to saccharin. After 8-weeks of the high-fat diet, OP rats had significantly greater weight gain and lower demand elasticity for sucrose and saccharin and higher demand intensity for saccharin. The changes in sucrose and saccharin elasticity suggest that DIO-induced changes in food-related behavior are associated with changes in reward processes. The changes in demand intensity for saccharin suggest that demand intensity, as a measure of ‘set point’, is not directly linked to metabolic processes. The current study shows that microeconomic theory and demand analysis is able to isolate independent aspects of diet-induced reward changes related to caloric and non-caloric reinforcers.

Introduction

Obesity is a growing world-wide problem with incidence in adults nearly tripling since 1975 [55] .To date, the majority of research on obesity has focused on the metabolic aspects (i.e., caloric intake and macronutrient distribution, hormonal signaling). However, recent evidence suggests that reward-related factors and associated brain changes also may play a role in obesity [52]. For example, obese individuals exhibit similarities in behavior relative to those with substance use disorders, although the focus is food rather than drug. Specifically, obese individuals show a lack of control over eating, difficulty achieving satiety, and an increased preoccupation with food [18,51]. Further, decreased dopamine D2 receptor signaling in the dorsal and ventral striatum as well as decreased baseline glucose metabolism in the prefrontal cortex are found in both those with substance use disorders and obese individuals [21,30,38,48,52,53]. Thus, reward-related brain dysfunctions may be related to the development and maintenance of obesity. However, the relative importance of reward-related vs. metabolic aspects of obesity currently is unknown. Specifically isolating the reward aspects of obesity from the metabolic aspects will further our understanding of the etiology. Isolation of the reward aspects of obesity from the metabolic aspects (here specifically food nutrient content) may be accomplished by systematically comparing the value changes in a caloric reinforcer such as sucrose to those of a non-caloric reinforcer such as saccharin [45]. Saccharin is non-caloric and does not directly alter metabolism or energy balance [47]. Thus, a change in saccharin value, as a function of diet, amount of diet consumed, and weight gain, is related more directly to changes in reward sensitivity.