Estudo de influências nutricionais na osteogênese e na odontogênese do rato (Rattus norveqicus albinus, Wistar)

Tese (Doutorado) — Universidade de Brasília, Faculdade de Ciências da Saúde, Programa de Pós-Graduação em Ciências Da Saúde, 2005.Realizou-se um estudo para verificar o papel dos nutrientes na osteogênese e na odontogênese do rato . A amostra consistiu de 22 ratos , 11 do grupo controle e 11 do grupo tratado analisados após um período de 7,14 e 21 dias . No grupo controle, os ratos foram amamentados por mães que utilizaram dietas normais em cálcio e fósforo durante a gestação. No grupo tratado, estes foram amamentados por mães cuja dieta continha valores reduzidos destes dois nutrientes. Após o sacrifício foram coletados os fêmures para análise pela técnica de calcinação, e os fêmures e cabeças para estudo histológico. Pôde-se concluir que a redução do cálcio e fósforo durante a gestação promoveu uma diminuição do peso e altura dos ratos. Observaram -se valores normais nos percentuais de cálcio e fósforo dos ossos, porém, com atraso na ossificação. Quanto à odontogênese, a formação de esmalte, pré-dentina e dentina também mostrou-se dentro dos padrões de normalidade . Apenas a rizogênese desenvolveu-se de forma mais lenta, interferindo no irrompimento dos dentes.It was conducted the present study with the objective to investigate the role of nutrients in rats’ osteogenesis and odontogenesis . Study sample was constituted by 22 rats, being 11 from the control group and 11 from the treated group, all of them analized after a peiod of 7, 14 and 21 days. In the control group, rats was fed by mothers using a normal calcium and phosphorus diet during pregnancy. In the treated group, rats were fed by mothers that, during their pregnancy .were submitted to a diet with reduced quantities of these two elements. When the rats were sacrificed, it was analized the femurs by the calcination process and by histologic study. The heads also was submitted to histologic study. Results indicated that calcium and phosphorus deprivation during pregnancy led to a reduction in rats’ weight and height . It was observed normal values in bones concentrations of calcium and phosphorus , but with a delay in ossification. Regarding odontogenesis , the formation of enamel, dentin ande pre- dentin was between normal values. Only root formation envolved in a more slow fashion, interfering in teeth arise

Chronic hyperpalatable diet induces impairment of hippocampal-dependent memories and alters glutamatergic and fractalkine axis signaling

Abstract Chronic consumption of hyperpalatable and hypercaloric foods has been pointed out as a factor associated with cognitive decline and memory impairment in obesity. In this context, the integration between peripheral and central inflammation may play a significant role in the negative effects of an obesogenic environment on memory. However, little is known about how obesity-related peripheral inflammation affects specific neurotransmission systems involved with memory regulation. Here, we test the hypothesis that chronic exposure to a highly palatable diet may cause neuroinflammation, glutamatergic dysfunction, and memory impairment. For that, we exposed C57BL/6J mice to a high sugar and butter diet (HSB) for 12 weeks, and we investigated its effects on behavior, glial reactivity, blood–brain barrier permeability, pro-inflammatory features, glutamatergic alterations, plasticity, and fractalkine-CX3CR1 axis. Our results revealed that HSB diet induced a decrease in memory reconsolidation and extinction, as well as an increase in hippocampal glutamate levels. Although our data indicated a peripheral pro-inflammatory profile, we did not observe hippocampal neuroinflammatory features. Furthermore, we also observed that the HSB diet increased hippocampal fractalkine levels, a key chemokine associated with neuroprotection and inflammatory regulation. Then, we hypothesized that the elevation on glutamate levels may saturate synaptic communication, partially limiting plasticity, whereas fractalkine levels increase as a strategy to decrease glutamatergic damage