Excessive consumption of highly palatable foods rich in sugar and fat, often referred to as "junk" or "fast" foods, plays a central role in the development of obesity. The highly palatable characteristics of these foods activate hedonic and motivational mechanisms to promote food-seeking behavior and overeating, which is largely regulated by the brain reward system. Excessive junk food consumption can alter the functioning of this reward system, but exact mechanisms of these changes are still largely unknown. This study investigated whether long-term junk food consumption, in the form of Cafeteria (CAF) diet, can alter the reward system in adult, female Long-Evans rats, and whether different regimes of CAF diet influence the extent of these changes. To this end, rats were exposed to a 6-week diet with either standard chow, or ad libitum daily access to CAF diet, 30 % restricted but daily access to CAF diet, or one-day-a-week (intermittent) ad libitum access to CAF diet, after which c-Fos expression in the Nucleus Accumbens (NAc), Prefrontal Cortex (PFC), and Ventral Tegmental Area (VTA) following consumption of a CAF reward of choice was examined. We found that all CAF diet regimes decreased c-Fos expression in the NAc-shell when presented with a CAF reward, while no changes in c-Fos expression upon the different diet regimes were found in the PFC, and possibly the VTA. Our data suggests that long-term junk food exposure can affect the brain reward system, resulting in an attenuated activity of the NAc-shell.
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http://dx.doi.org/10.1016/j.physbeh.2024.114478 | DOI Listing |
Am J Physiol Gastrointest Liver Physiol
January 2025
Digestive Diseases, Emory University, Atlanta, GA, United States.
The interplay between diet-induced obesity and gastrointestinal dysfunction is an evolving area of research with far-reaching implications for understanding the gutbrain axis interactions. In their study, Ramírez-Maldonado et al. employ a cafeteria (CAF) diet model to investigate the effects on gut microbiota, enteric nervous system (ENS) integrity and function, and gastrointestinal motility in mice.
View Article and Find Full Text PDFBiomedicines
January 2025
Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Colima 28045, Colima, Mexico.
In recent years, the role of neurotrophins and their receptors in peripheral tissues has been of great interest. At a metabolic level, the brain-derived neurotrophic factor (BDNF) and its receptor trkB have been reported to participate in insulin secretion from the pancreas in response to increases in circulating blood glucose. To determines the role of the BDNF-trkB pathway in insulin secretion and pancreatic morphology in rats fed a cafeteria-style diet for 16 weeks.
View Article and Find Full Text PDFBiofactors
January 2025
Departament de Bioquimica i Biotecnologia, Universitat Rovira i Virgili, Nutrigenomics Research Group, Tarragona, Spain.
Current lifestyles include calorie-dense diets and late-night food intake, which can lead to circadian misalignment. Our group recently demonstrated that sweet treats before bedtime alter the clock system in healthy rats, increasing metabolic risk factors. Therefore, we aimed to assess the impact of the sweet treat consumption time on the clock system in rats fed a cafeteria diet (CAF).
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Biology and Biotechnologies "Charles Darwin", Sapienza University, 00185, Rome, Italy.
Background: Metabolic syndrome represents a pancreatic ductal adenocarcinoma (PDAC) risk factor. Metabolic alterations favor PDAC onset, which occurs early upon dysmetabolism. Pancreatic neoplastic lesions evolve within a dense desmoplastic stroma, consisting in abundant extracellular matrix settled by cancer associated fibroblasts (CAFs).
View Article and Find Full Text PDFDiseases
December 2024
Centro de Investigaciones Biomédicas, Doctorado en Ciencias Biomédicas, Universidad Veracruzana, Xalapa 91190, Mexico.
Introduction: Consuming hypercaloric diets during pregnancy induces metabolic, immune, and maternal intestinal dysbiosis disorders. These conditions are transferred to the offspring through the placenta and breastfeeding, increasing susceptibility to metabolic diseases. We investigated the effect of GG supplementation on offspring maternally programmed with a hypercaloric diet.
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