Perinatal and post-weaning exposure to a high-fat diet causes histomorphometric, neuroplastic, and histopathological changes in the rat ileum.

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.

Exposure to a high-fat diet during intrauterine life and post-birth causes cardiac histomorphometric changes in rats: A systematic review.

Cardiac histomorphometric changes are conditions present as an adaptive response to increased cardiovascular demand, such as in obesity or the consumption of a high-fat diet. Epidemiologic studies show an increase in maternal obese individuals, with repercussions on offspring cardiovascular health. OBJECTIVE: The goal of this study was to systematically review studies that evaluated cardiac histomorphometric changes in rodents exposed to a high-fat diet. DATA SOURCE: PubMed, Embase, Science Direct, Web of Science and Lilacs. DATA EXTRACTION: Animal species, percentage of dietary fat, period and time of exposure and main cardiac change results were extracted. DATA ANALYSIS: A total of 1687 studies were found, and 20 met the inclusion criteria for this systematic review. A maternal high-fat diet was started 3 to 4 weeks before mating in most (70%) of the studies. Nutritional manipulation of offspring was initiated during pregnancy and maintained until the end of lactation in most (45%) of the studies. The fat percentage of high-fat diets ranged between 20% and 62%. The studies showed increases in cardiomyocytes, left ventricle size, and whole heart hypertrophy. Some studies showed increased thickness of the middle intima layer of the aorta and atherosclerosis. Studies that maintained a high-fat diet after the lactation period also showed an increase in cardiac hypertrophy. CONCLUSION: Maternal exposure to a hyperlipidic diet in the fetal stages of cardiac development causes cardiac hypertrophy in offspring. The high variation in the dietary fat and the difference in the time and period of exposure of the offspring to the high - fat diet suggest the high degree of sensitivity of the cardiac structure.

High-fat diet promotes hypothalamic inflammation in animal models: a systematic review.

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.

Does a high-fat diet-induced obesity model brown adipose tissue thermogenesis? A systematic review.

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.

Housing Temperature Modulates the Impact of Diet-Induced Rise in Fat Mass on Adipose Tissue Before and During Pregnancy in Rats.

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.