TABLE I. Absorption of Egg Yolk-Bound 57C0 Vitamin B,, Administered as an Omelette or an Eggnogreticulocyte count in myelodysplasia is compai-able to the values for healthy subjects (men and women) (see Table I).Some of the patients suffering from severe anemia in inyelodyaplasia received blood transfusions but these did not change significantly the reticulocyte count and HFR.In contra\t to a normal reticulocyte count, the niean HFR ratio and the r ratio are found to be higher in patients with myelodysplasia. Concerning the r ratio. the difference between the group of healthy donors and the group of patients with myelodysplasia is highly significant ( P < 0.001) (Table I) but the difference between the subgroups of myelodysplasia is not significant (data not shown).In myelodysplasia. the global count ofrcticulocytes is of little help iii the evaluation of bone inarrow activity. The discrepancy between a high ratio HFR and a normal reticulocyte count remains difficult to assess in myelodysplasia. Lofters et al. 141 have reported a case of preleukemia with in vitro evidence of abnormal reticulocyte maturation. The patient had marked reticulocytosis apparently caused by a delayed maturation of all the subgroups of reticulocytes. Lofters et al. wggest that this could be due to abnormal ribonucleic acid or to a quantitative or qualitative deficiency of ribonuclease.In our study, a higher r index ruggests an abnonnal reticulocyte maturation, with a prolonged survival of younger reticulocytes. fnllowed by a reticulocyte abortion. resulting in a normal or low reticulocyte count, these phenomena leading to a nonregenerative anemia. These data suggest that r could be evaluated as another indice of erythropoiesis in nonregenerative anemia in order to give further evidence of a putative myelodysplastic syndrome.
This mode of action of leucine was studied using rat tissues. Leucine slightly increased the glucose uptake and glycogen deposition by the fasted rat diaphragm. Leucine did not potentiate the effect of insulin. Tolbutamide, but not leucine, increased insulin release by the whole rat pan¬ creas. Hepatic glucose output in the perfused normal fed rat liver was inhibited by 20% when leucine was added to the perfusion, but a constant infusion of insulin did not change the hepatic glucose output. Leucine produced a similar per cent decrease in hepatic glucose output in rat liver slices. The hypoglycémie effect of leucine is not con¬ sidered to be due to any peripheral effect per se or to a protentiation of a peripheral insulin effect. A direct pan¬ creatic effect of leucine was not demonstrated in these ex¬ periments. The inhibition of hepatic glucose output may be one of the major factors involved in leucine-induced hypo¬ glycémie. Reversible Defect in Renal Ammonium Excretion in PatientsWith Hypercalcemia\p=m-\H.O. Heinemann Metabolism 12:792 (Sept) 1963 The effect of hypercalcemia on renal ammonium excretion was studied in nine patients with various neoplasms and one with hyperparathyroidism. The results demonstrate that hypercalcemia leads to a potentially reversible defect In ammonium excretion. The defect is not due to a limited diffusion gradient for ammonia between the tubular cells and the tubular lumen, because titrable acid excretion and lowering of the urine pH are not impaired. The defect is also not due to concomitant metabolic alkalosis because it occurs in the absence of metabolic alkalosis and is not cor¬ rected by prolonged administration of acidifying salts. The exact nature of the reversible defect in ammonium excretion remains unexplained.Metabolism 12:804 (Sept) 1963 Studies were conducted to delineate the renal mechanism of reduction in the rate of sodium excretion by glucose after fasting. Initially, solute diuresis produced with glucose did not differ from mannitol diuresis. However, after a lag period of 2 hours, sodium excretion was lower at all rates of solute clearance during a similar glucose diuresis, and venal concentrating ability was increased simultaneously. These effects were independent of body sodium content. Mechanisms are discussed whereby reduction in sodium ex¬ cretion will augment renal concentrating ability. It is sug¬ gested that in fasted subjects glucose acts to increase sodium reabsorption from distal portions of the nephron into the renal medulla, thus decreasing sodium excretion and augmenting renal concentrating ability. Effects of Epinephrine on Free Fatty Acid Mobilization in Hyperthyroid and Hypothyroid Subjects\p=m-\J.Hamburger, R. W. Smith. Jr., and J. M. Miller Metabolism 12:821 (Sept) 1963 Since epinephrine is a potent lipolytic hormone and the level of thyroid function conditions its hyperglycémie and hemodynamic actions, hyperthyroid, hypothyroid and euthyroid subjects were compared in respect to free fatty acid ( FFA ), and in some instances glucose, respo...
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