RESUMO
Exposure to a diet with a high saturated fat content can influence the characteristics of the gastrointestinal tract, causing losses in the absorption of nutrients and favoring the appearance of diseases. The objective was to assess the effects of a high-fat diet (HFD) in the perinatal (pregnancy and lactation) and post-weaning period on the histomorphometry, neuroplasticity, and histopathology of the ileum. Wistar rats were divided into four subgroups: Control/Control (CC, n = 10) rats fed a control diet (C) throughout the trial period; Control/HFD (CH, n = 9) rats fed diet C (perinatal) and HFD after weaning; HFD/Control (HC, n = 10) rats fed HFD (perinatal) and diet C (post-weaning); HFD/HFD (HH, n = 9) rats fed HFD throughout the experimental period. There was atrophy of the Ileum wall with a reduction in the muscular tunic, submucosa, and mucosa thickness in the HH group of 37%, 28%, and 46%, respectively (p < 0.0001). The depth of the crypts decreased by 29% (p < 0.0001) and height increased by 5% (p < 0.0013). Villus height decreased by 41% and 18% in HH and HC groups (p < 0.0001) and width decreased by 11% in the HH (p < 0.0001). The height of the enterocytes decreased by 18% in the HH (p < 0.0001). There was a decrease in the area of the myenteric and submucosal plexus ganglia in the HH and HC groups (p < 0.0001). The number, occupation, and granules of Paneth cells increased in the HH and HC groups (p < 0.0001). Intraepithelial lymphocytes (IELs) increased in all groups exposed to the HFD. Goblet cells decreased in groups CH and HH (p < 0.0001). The evidence from this study suggests that the HFD had altered the histomorphometry, neuroplasticity, and histopathology of the ileum of the rats.
Assuntos
Dieta Hiperlipídica , Ácidos Graxos , Gravidez , Feminino , Ratos , Animais , Dieta Hiperlipídica/efeitos adversos , Desmame , Ratos Wistar , ÍleoRESUMO
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.
Assuntos
Dieta Hiperlipídica , Hipotálamo , Animais , Biomarcadores/metabolismo , Citocinas , Dieta Hiperlipídica/efeitos adversos , Humanos , Hipotálamo/metabolismo , Inflamação/etiologia , Inflamação/metabolismoRESUMO
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.