ABSTRACT
CONTEXT: Hypothalamic inflammation and dysfunction may be induced by high-fat diets. However, the mechanisms involved in this process have not been fully elucidated. OBJECTIVE: To evidence, in animal models, of how a high-fat diet influence the mechanisms involved in hypothalamic inflammation. DATA SOURCES: Scopus, PubMed/Medline, Web of Science, Science Direct, and Embase databases were searched. DATA EXTRACTION: The exclusion criteria were human studies, studies with medicinal products or other substances not related to food, paper reviews, studies that used a surgical intervention or an intervention with food to reverse hypothalamic inflammation, and studies with genetically modified animals. The identified studies were evaluated according to the following inclusion criteria: animal studies, studies in which a control group was included in the experimental design, and studies in which markers of inflammation in the hypothalamus were evaluated. DATA ANALYSIS: A total of 322 studies were found, of which 9 met the inclusion criteria for a systematic review, conducted in accordance with the PRISMA guidelines, and were included in this review. CONCLUSION: The exposure of rodents to high-fat diets promoted an increase in levels of several pro-inflammatory cytokines and other proteins involved in the inflammatory process in the hypothalamus. This process was associated with increased glial cell activity.
Subject(s)
Diet, High-Fat , Hypothalamus , Animals , Biomarkers/metabolism , Cytokines , Diet, High-Fat/adverse effects , Humans , Hypothalamus/metabolism , Inflammation/etiology , Inflammation/metabolismABSTRACT
INTRODUCTION: In this systematic review, we analysed studies that assessed the brown adipose tissue (BAT) activity in the high-fat/cafeteria diet model of obesity in rats. MATERIAL AND METHODS: Scopus, PubMed, Embase, and ScienceDirect databases were searched from January 2017 to November 2017. Using specific combinations of medical subject heading (MeSH) descriptors, seven papers remained after the inclusion and exclusion criteria. RESULTS: Most papers showed an increase in BAT thermogenesis in rodents fed high-fat/cafeteria diet. Some studies did not mention the diet composition or housing temperature, and the most of them investigated the thermogenesis superficially, being limited to the analysis of the UCP 1 expression. CONCLUSIONS: Despite the consolidated use of high-fat/cafeteria diets as a model to induce obesity, the identification of the energy expenditure arm has been slow, especially the direct quantitative assessment of the contribution of BAT to the increase in metabolic rate in rats fed a cafeteria/high-fat diet.
ABSTRACT
Aim: To investigate whether housing temperature influences rat adiposity, and the extent it is modified by diet and/or pregnancy. Housing temperature impacts on brown adipose tissue, that possess a unique uncoupling protein (UCP) 1, which, when activated by reduced ambient temperature, enables rapid heat generation. Methods: We, therefore, examined whether the effects of dietary induced rise in fat mass on interscapular brown fat in female rats were dependent on housing temperature, and whether pregnancy further modulates the response. Four week old rats were either maintained at thermoneutrality (27°C) or at a "standard" cool temperature (20°C), and fed either a control or obesogenic (high in fat and sugar) diet until 10 weeks old. They were then either tissue sampled or mated with a male maintained under the same conditions. The remaining dams were tissue sampled at either 10 or 19 days gestation. Results: Diet had the greatest effect on fat mass at thermoneutrality although, by 19 days gestation, fat weight was similar between groups. Prior to mating, the abundance of UCP1 was higher at 20°C, but was similar between groups during pregnancy. UCP1 mRNA followed a similar pattern, with expression declining to a greater extent in the animals maintained at 20°C. Conclusion: Housing temperature has a marked influence on the effect of dietary induced rise in fat deposition that was modified through gestation. This maybe mediated by the reduction in UCP1 with housing at thermoneutrality prior to pregnancy and could subsequently impact on growth and development of the offspring.
