High-fat diet alters weight, caloric intake, and haloperidol sensitivity in the context of effort-based responding

Abstract

High-fat (HF) diets result in weight gain, hyperphagia, and reduced dopamine D2 signaling; however, these findings have been shown only under free-feeding conditions. This study tested the extent to which HF diet affects effort-dependent food procurement and the extent to which dopamine signaling is involved. Male Sprague-Dawley rats consumed either a HF (n = 20) or standard-chow (n = 20) diet. We assessed sensitivity to effort-based reinforcement in ten rats from each group by measuring consumption across a series of fixed-ratio schedules (FR 5 – FR 300) under a closed economy, and quantified performance using the exponential demand equation. For each FR, acute injections of 0 or 0.1 mg/kg of haloperidol, a D2 antagonist, were administered to assess dopamine-related changes in consumption. Rats fed a HF diet consumed more calories and weighed significantly more than rats fed standard chow. Food consumption decreased in both groups in an effort-dependent manner, but there were no group differences. Haloperidol reduced responding in a FR-dependent manner for both groups. Animals exposed to a HF diet showed an altered sensitivity to haloperidol relative to rats fed a standard diet, suggesting that HF diet alters sensitivity to DA signaling underlying effort-based food procurement.

Effects of a cafeteria diet on delay discounting in adolescent and adult rats: Alterations on dopaminergic sensitivity

“…Within each age group, rats fed a cafeteria diet gained more weight relative to rats fed a standard diet. These findings support research that DIO results in excessive weight gain and higher caloric intake compared to standard diet controls (Boomhower and Rasmussen, 2014; Johnson and Kenny, 2010; Robertson et al, 2017; Rolls et al, 1980).…”

“…Researchers found no baseline differences in delay discounting as a function of diet; however, rats fed a high-fat diet were more sensitive to acute injections of haloperidol (a D 2 antagonist), such that they showed higher impulsivity under haloperidol than rats fed a standard diet. These changes are consistent with diet-related changes that affect D 2 structure and function in the brain (Baladi, et al, 2012; Boomhower and Rasmussen, 2014; Geiger et al, 2009; Johnson and Kenny, 2010; Robertson et al, 2017; Val-Laillet et al, 2011; Vucetic et al, 2012).…”

“…Using the rats with the highest (DIO) and lowest (standard diet) body weights is a standard practice (e.g. Boomhower and Rasmussen, 2014; Huang et al, 2003; 2006; Johnson and Kenny, 2010; Levin and Keesey, 1998; Robertson et al, 2017) used to maximize the differences in weights and D 2 in the striatum between groups (Johnson and Kenny, 2010; Wang et al, 2001), as well as to ensure that the animals were a model of obesity, and not simply an evaluation of the effects of a cafeteria diet, per se. The Idaho State University Institutional Animal Care and Use Committee approved all procedures.…”

“…Second, high-fat diets, compared to control diets, can directly alter dopaminergic brain reward areas, via downregulation of D 2 receptor densities in the striatum (Johnson and Kenny, 2010), reductions of DA in the NAc shell (Geiger et al, 2009), and lower dopamine D 2 receptor gene expression in the VTA (Vucetic et al, 2012). Third, a high-fat diet can alter behavioral sensitivity to dopaminergic D 2 compounds in behavioral economic tasks that use food as a reinforcer (Boomhower and Rasmussen, 2014; Robertson et al, 2017). Taken together, these studies demonstrate that diet can influence dopaminergic D 2 function in the brain, especially in areas involved in reward.…”

Translating Behavior Analysis: a Spectrum Rather than a Road Map

“…Any experiment that investigates the behavior of a nonhuman animal model of human disordered behavior or disease processes is T1 provided that the research question is related to the disorder or disease. For example, compared to a "standard" diet, a diet that is high in fat resulted in increased food consumption and body mass (among other results) in rats in both free-feeding (Boomhower & Rasmussen, 2014) and effort-based (Robertson, Boomhower, & Rasmussen, 2017) contexts. Demonstrating similar effects conclusively in humans has been slow, challenging, and notoriously controversial (e.g., Taubes, 2013).…”