Efeito da deficiência de energia na dieta sobre a população de protozoários ciliados do rúmen de bovinos

Ten young rumen-cannulated crossbred steers were randomly divided into two groups: a control group (C; n=4), which was fed a balanced diet for daily weight gain of 900g; and a pronounced energy-deprived group (PED; n=6), receiving 30% less of the required energy for maintenance. After 140 days of these alimentary regimes, rumen fluid and urine samples were collected for biochemical and functional tests, before feeding and at 1, 3, 6, and 9 hours after feeding. The energy-deprivation diet caused a significant reduction in the number of Entodinium, Eodinium, Isotricha, Dasytricha, Eremoplastron, Eudiplodinium, Metadinium, Charonina, Ostracodinium, and Epidinium protozoa. There was no effect of the time of sampling in both groups on the total number of ciliates in rumen fluid. A higher number of protozoan forms in binary division were recorded in the control group, at the 6th and 9th hours after feeding (P<0.019). There was a high positive correlation between the total count of protozoans in rumen fluid and glucose fermentation, ammonia, and urinary allantoin excretion index; and a negative correlation between the total count of protozoa and metilene blue reduction, and a medium correlation between the total count of protozoa and total volatile fatty acids concentration. The determination of the protozoa populations does not imply in the use of complex and hard-to-execute techniques, although it is time consuming and needs practice. This exam particularly helps in clinical expected diagnosis.Foram utilizados 10 novilhos mestiços com cânula ruminal, distribuídos em dois grupos: no grupo controle (C; n=4) receberam dieta balanceada para ganho diário de 900g; no grupo tratado com carência pronunciada de energia (CP; n=6), receberam dieta com 30% a menos do nível de mantença em energia. Após 140 dias sob esses regimes de alimentação, foram coletadas amostras do fluido ruminal e urina, para realização de provas bioquímicas e funcionais, antes e às 1, 3, 6 e 9 horas após o fornecimento do alimento. A carência energética resultou em diminuição significativa na quantidade dos protozoários Entodinium, Eodinium, Isotricha, Dasytricha, Eremoplastron, Eudiplodinium, Metadinium, Charonina, Ostracodinium e Epidinium. Não houve efeito da hora de coleta sobre o total de ciliados nos grupos C e CP. Maior número de formas em divisão binária foi registrado no grupo C, na sexta e nona horas pós-alimentação (P<0,019). Observaram-se altas correlações positivas entre a contagem total de protozoários e a fermentação de glicose, amônia e o índice de excreção urinária de alantoína e negativa entre a contagem total de protozoários e a redução do azul de metileno, e correlação média entre a contagem total de protozoários e os ácidos graxos voláteis totais. A determinação da população de protozoários do rúmen é um método simples de avaliação, além de que particularmente auxilia o diagnóstico clínico da função ruminal

Selected ruminal variables and purine urinary excretion rate of steers subjected to feeding, fasting, and re-feeding conditions

The effects of feeding, fasting, and re-feeding on the ruminal profile of growing cattle were studied. Ruminal fluid and urine samples were obtained from 12 crossbred steers weighing approximately 300 kg during the following periods: 11 h of normal feeding (postprandial period), 48 consecutive hours of fasting, and followed by 48 h of re-feeding. Fasting promotes changes in the ruminal profile, such as an increase in ruminal pH, reduction in the number of rumen protozoa and bacteria, and decrease in the urinary excretion of allantoin; however, it does not change the urinary uric acid excretion rate. The overall mean ruminal pH was higher during fasting (7.53±0.27) in comparison to those at normal feeding (6.72±0.25) and re-feeding (6.62±0.31) (p&lt;0.05). During re-feeding, the ruminal profile returned to normal, except for the protozoa count, which despite a slight increase only after 48 h of re-feeding, did not recover to baseline values

Genetic and biochemical markers in patients with Alzheimer's disease support a concerted systemic iron homeostasis dysregulation

Alzheimer's disease (AD) is the most common form of dementia in the elderly individuals, resulting from a complex interaction between environmental and genetic factors. Impaired brain iron homeostasis has been recognized as an important mechanism underlying the pathogenesis of this disease. Nevertheless, the knowledge gathered so far at the systemic level is clearly insufficient. Herein, we used an integrative approach to study iron metabolism in the periphery, at both genotypic and phenotypic levels, in a sample of 116 patients with AD and 89 healthy control subjects. To assess the potential impact of iron metabolism on the risk of developing AD, genetic analyses were performed along with the evaluation of the iron status profile in peripheral blood by biochemical and gene expression studies. The results obtained showed a significant decrease of serum iron, ferritin, and transferrin concentrations in patients compared with the control subjects. Also, a significant decrease of ferroportin (SLC40A1) and both transferrin receptors TFRC and TFR2 transcripts was found in peripheral blood mononuclear cells from patients. At the genetic level, significant associations with AD were found for single nucleotide polymorphisms in TF, TFR2, ACO1, and SLC40A1 genes. Apolipoprotein E gene, a well-known risk factor for AD, was also found significantly associated with the disease in this study. Taken together, we hypothesize that the alterations on systemic iron status observed in patients could reflect an iron homeostasis dysregulation, particularly in cellular iron efflux. The intracellular iron accumulation would lead to a rise in oxidative damage, contributing to AD pathophysiology

Alterações fenotípicas e genéticas do metabolismo do ferro numa população portuguesa com doença de Alzheimer: potenciais implicações no conhecimento da fisiopatologia e no diagnóstico desta demência

Fundação Astrazeneca e INSA, I.P