The effect of increasing phosphorus (P) intake on P utilization was investigated in balance experiments using 12 Saanen goats, 4 to 5 mo of age and weighing 20 to 30 kg. The goats were given similar diets with various concentrations of P, and 32P was injected to trace the movement of P in the body. A P metabolism model with four pools was developed to compute P exchanges in the system. The results showed that P absorption, bone resorption, and excretion of urinary P and endogenous and fecal P all play a part in the homeostatic control of P. Endogenous fecal output was positively correlated to P intake (P < .01). Bone resorption of P was not influenced by intake of P, and P recycling from tissues to the blood pool was lesser for low P intake. Endogenous P loss occurred even in animals fed an inadequate P diet, resulting in a negative P balance. The extrapolated minimum endogenous loss in feces was .067 g of P/d. The minimum P intake for maintenance in Saanen goats was calculated to be .61 g of P/d or .055 g of P/(kg(.75) x d) at 25 kg BW. Model outputs indicate greater P flow from the blood pool to the gut and vice versa as P intake increased. Intake of P did not significantly affect P flow from bone and soft tissue to blood. The kinetic model and regressions could be used to estimate P requirement and the fate of P in goats and could also be extrapolated to both sheep and cattle.
-The effect of glycemic state on status epilepticus (SE) development was studied in animals of d i ff e rent ages, submitted to pilocarpine model of epilepsy. Groups: I-Rats with 9-day-old (P9): IA. Submitted to 1SE; IB. Saline-treated; IC. Induced-hyperglycemia; ID. Induced-hyperglycemia+SE; II-Rats submitted to t h ree consecutive episodes of SE at P7, P8 and P9; III-Rats submitted to 1SE at P17; IV-Rats submitted to 1SE at P21. Hippocampal cell death and the expression of glucose transporter GLUT3 were analyzed in g roup I. The results demonstrated normoglycemia in the groups IA, IB and II, hypoglycemia in group III and hyperglycemia in group IV, showing that the glycemia during SE is age dependent . Induced hyperglycemia during SE in P9 protected the hippocampal neurons from death and both groups IC and ID presented increased GLUT3 expression, showing high glucose consumption by the hippocampus.KEY WORDS: status epilepticus, pilocarpine, glycemia, hippocampus, glucose transporter 3.Efeito do estado glicêmico em ratos submetidos ao status epilepticus durante o desenvolvimento
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