“Liking” and “wanting” of sweet and oily food stimuli as affected by high-fat diet-induced obesity, weight loss, leptin, and genetic predisposition

Abstract

Cross-sectional studies in both humans and animals have demonstrated associations between obesity and altered reward functions at the behavioral and neural level, but it is unclear whether these alterations are cause or consequence of the obese state. Reward behaviors were quantified in male, outbred Sprague-Dawley (SD) and selected line obesity-prone (OP) and obesity-resistant (OR) rats after induction of obesity by high-fat diet feeding and after subsequent loss of excess body weight by chronic calorie restriction. As measured by the brief access lick and taste-reactivity paradigms, both obese SD and OP rats "liked" low concentrations of sucrose and corn oil less, but "liked" the highest concentrations more, compared with lean rats, and this effect was fully reversed by weight loss in SD rats. Acute food deprivation was unable to change decreased responsiveness to low concentrations but eliminated increased responsiveness to high concentrations in obese SD rats, and leptin administration in weight-reduced SD rats shifted concentration-response curves toward that seen in the obese state in the brief access lick test. "Wanting" and reinforcement learning as assessed in the incentive runway and progressive ratio lever-pressing paradigms was paradoxically decreased in both obese (compared with lean SD rats) and OP (compared with OR rats). Thus, reversible, obesity-associated, reduced "liking" and "wanting" of low-calorie foods in SD rats suggest a role for secondary effects of the obese state on reward functions, while similar differences between select lines of OP and OR rats before induction of obesity indicate a genetic component.

Metabolic programming effects initiated in the suckling period predisposing for adult-onset obesity cannot be reversed by calorie restriction

“…This observation is in concurrence with the report that CR causes reductions in body weight and normalization of blood glucose and hormone levels in obese animals as well as in nonhuman primates (35). Another study showed that CR reversed the alterations in taste-guided responsiveness that was induced by high-fat diet feeding in rats (28). The pair-feeding regimen imposed on the HC rats involved restriction of rodent chow for the HC/PF rats on a daily basis from the time of weaning, whereas CR in other animal models involved food restriction ranging from 20 to 40% during the period of investigation and in most studies was imposed on older animals.…”

Taste of Fat: A Sixth Taste Modality?

“…Therefore, it is tempting to speculate that GLP-1 increases the "fatty" taste sensitivity by participating in the dynamic regulation of lingual CD36 during the prandial period (121). Conversely, systemic leptin injection reduces a behavioral response to low corn oil concentrations, compared with saline injection, in rats subjected to brief-access licking tests (192). Finally, a regulatory loop linking LCFA, endocannabinoids, and preference for fat has also been recently identified in the rat (40).…”

The oral lipid sensor GPR120 is not indispensable for the orosensory detection of dietary lipids in mice

“…by guest, on May 11, 2018 www.jlr.org Downloaded from measure taste-guided reward behavior [i.e., hedonic value and motivation ( 27 )]. Therefore, computer-controlled lickometers were used to measure the number of licks for 1 min and determine the attraction for 0.5% OLA or 0.5% LA solubilized in mineral oil.…”