In Rats Fed High-Energy Diets, Taste –Rather than Fat Content– Is the Key Factor Increasing Food Intake. Comparison of a Cafeteria and a Lipid-Supplemented Standard Diet (Raw data)

Dades primàries associades a un article enviat a la revista PeerJ i pendent d'avaluació (maig 2017)Podeu consultar l'article a: http://hdl.handle.net/2445/115482Background: Diet deeply affects the food selection and ingestion both in humans and rodents, often resulting in excess energy intake. Methods: We investigated this process comparing two different high-fat dietary approaches to induce obesity, in which all rats received about 40% of their energy intake as lipids. The main nutrient difference between the diets, when compared with controls fed standard lab chow, was the lipid content. Cafeteria diets (K) were devised to be tasty, and thus highly desirable to the rats, mainly for its diverse mix of tastes, particularly salty and sweet. This diet was compared with another high-fat (HF) potentially obesogenic diet, devised not to be as tasty as K, and prepared just supplementing standard chow pellets with fat. We also analysed the influence of sex on the effects of the diets. Results: K rats grew faster, especially the males, although females showed a higher proportion of body lipid, because of a high lipid, sugar and protein intake. HF weight change rates were not different from those of controls. In addition to high sugar, K rats also ingested large amounts of salt. With this study we have shown that the key factor eliciting the excess energy intake in a high-energy diet rat model was not solely or mainly their fat intake. The changes in body fat accrual were more a consequence of their appetence for the food. Conclusions: The results show that the significant presence of sugar and salt is a powerful factor promoting excess food intake, more effective than increasing diet lipid content. These effects were already observed after a relatively short treatment, additionally confirming the differential effects of sex on the hedonic and obesogenic response to diet