摘要:

SummaryThe aim of the study was to develop an animal model of steroid stunting and catch-up growth and to investigate the possibility that calcium supplements, with or without vitamin D supplements, might mitigate the effects of corticosteroids on linear growth.In the first experiment, newly weaned Wistar rats were allocated to four groups and weight and tail length measured weekly. In three groups cortisone was injected daily for 28 days. Two of the cortisone-treated groups were given calcium supplements daily in different dosage schedules. During cortisone treatment (Table 1), animals given cortisone gained less weight than the controls (P <0.01). After cortisone was stopped the groups previously given cortisone showed greater weight gain than the controls (P <0.01). Changes in tail length (Fig. 2), representing changes in linear growth, showed that groups receiving cortisone grew less than the controls during cortisone treatment. After cortisone was stopped the control group grew less than the three groups that had previously received cortisone. There was no beneficial effect of supplemental calcium on either the degree of growth retardation or of catch-up growth (Tables 1 and 2).A second experiment was performed to test the reproducibility of the method and to study the effects of calcium and vitamin D supplements on growth. Newly weaned rats were allocated to four groups. Three groups received cortisone for 42 days. Two of the cortisone-treated groups received vitamin D once a week and one of these groups received calcium supplements. Weight and tail length velocities (Figs. 5 and 6) show less velocity than that of the cortisone-treated groups during cortisone treatment, and after cortisone was stopped the control group had lesser velocity. During cortisone treatment (Table 3), the control groups gained more weight than the three groups given cortisone (P <0.001). After cortisone was stopped the groups previously receiving cortisone gained more weight than the control group (P <0.01 for cortisone alone and P <0.001 for cortisone and vitamin D). Changes in mean tail lengths (Table 4) show that during cortisone treatment the three groups given cortisone alone, cortisone and vitamin D, and cortisone, vitamin D, and calcium, all gained less than the controls (P <0.001). After cortisone was stopped the groups previously treated with cortisone had a greater increase in tail length than the control groups (P <0.001). The group given vitamin D supplements grew more than the group given cortisone without such supplements (P <0.01). The food consumed by the animals (g/100 g body wt/day) was measured (Fig. 7), and at no time did the control group eat more than the cortisone-treated groups. Reduced calorie intake was not the explanation for retardation of growth, and the increased food intake after cortisone was presumably necessary for catch-up. The serum calcium and total body calcium at the end of the experiment (Table 5) did not suggest that cortisone had depleted the skeleton of calcium.The experiment confirmed that cortisone inhibits growth of total body weight and of tail length in newly weaned rats, but the total growth of all groups was similar by the end of the experiment and confirmed that catch-up growth had occurred. The groups given vitamin D supplements had a greater increase in tail length in the catch-up phase than the group given cortisone without such supplements. It may be that vitamin D had a specific effect on the growth plate, ameliorating the effects of corticosteroids on growing cartilage.SpeculationThe growth retardation induced by cortisone may be partly related to direct effects on the skeleton. Vitamin D may improve catch-up growth by antagonizing the effects of corticosteroids on the growth plate.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SummaryAn intestinal perfusion technique has been used to study absorption of glucose from free glucose and the disaccharide maltose in a patient with congenital glucose-galactose malabsorption.Minimal absorption of glucose occurred from high luminal concentrations of either free glucose (100 mmole/liter) or maltose (50 mmole/liter). Glucose diffused into the intestinal lumen during perfusion of a 2 mmole/liter glucose solution.These observations offer no support for nutritionally important glucose absorption in congenital glucose-galactose malabsorption by either passive diffusion or via a “disaccharidase-related” transport system.SpeculationIn patients with congenital glucose-galactose malabsorption a disaccharidase-related transport system is of no importance as a physiologic mechanism in compensating for the primary defect of monosaccharide absorption.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SummaryIn order to determine unambiguously the presence of multiple forms of β-glucosidase in normal leukocytes and fibroblasts and the form(s) present in Gaucher's disease, we had to devise techniques to separate β-glucosidase from the lysosomal membrane in a catalytically active form and to visualize the isozymes electrophoreticaily. Separation of relatively stable enzyme from the membrane was not achieved until leukocyte and fibroblast suspensions were freeze-thawed consecutively 10 times. After Cellogel electrophoresis of normal leukocyte extracts, two distinct and discrete bands of β-glucosidase activity, which migrated toward the anode, were observed using the fluorogenic substrate 4-methylumbeIliferyl- β-D-glucopyranoside. In patients with juvenile onset Gaucher's disease, all of the leukocyte β-glucosidase activity remained at the origin. The electrophoretic pattern of β-glucosidase from normal cultured skin fibroblasts showed only one fluorescent band of β-glucosidase activity which also migrated toward the anode, but with lesser mobility than the leukocyte bands. In fibroblast extracts of patients with Gaucher's disease,β-glucosidase activity could not be visualized after electrophoresis, even though prior to electrophoresis these extracts had 15-35% of normal activity.In contrast to the enzyme from leukocytes and fibroblasts, β- glucosidase activity in the spleen and liver was easily release by homogenization. Only one band of β-glucosidase activity, more rapidaly anodal than the leukocyte isozmes, was ibserved after ekectriohoresis.Enyme acti ity in splenic crude homogenates from five patients with Gaucheresis, disease varied from 5.2-60.8% of normal. After electrophoresis, diminished activety of β-glucosidase with the same mobility as the normal enzyme was detected in the two spleen samples with highest activity.SpeculationThe electrophoretic behavior of leukocyte β-glucosidase from patients with juvenile onset Gaucher'disease suggests that the condition results from the synthesis of an altered enzyme, which is bound enzyme.The abnormal membrane binding could interfere with the accessibility of the enzyme to the natural substrate and account for the gradual accumulation of glycospingolipid in the patients.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SummaryThe transport of α-aminoisobutyric acid and α-methyl-D-glucoside by isolated renal tubules from Sprague-Dawley rats at different stages of development follows a separate age-dependent pattern for each substrate. The effects of 6 mM maleic acid on transport processes differ for amino acids and sugars and become manifest at distinct points during development. Maximum inhibition by maleic acid occurs at a time subsequent to maturity of these transport systems. In an effort to explain these transport phenomena, the uptake and metabolism of14C-labeled maleic acid by the newborn or adult renal tubule was studied, showing significant binding by the tubule membrane, penetration of the cell by diffusion, and no conversion to14CO2. Maleic acid has no demonstrable effect on the membrane-associated enzymes which are thought to play a role in the transport of small molecules.SpeculationAlthough the mechanism by which maleic acid inhibits the transport of sugars and amino acids hi the adult rat tubule preparation remains unexplained, it is clear that its effects are age-related and independent of the maturation of these transport systems. This observation is consistent with the delayed appearance of the Fanconi syndrome seen in human cystinosis, and suggests that the progressive tubular dysfunction in this syndrome and in the maleic acid model is secondary to genetically directed intracellular metabolic changes expressed during development.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SummaryConcentrative uptake of α-methyl-D-glucoside (AMG) by isolated renal tubule fragments from the newborn Sprague-Dawley rat has been demonstrated and the validity of this phenomenon confirmed by an in vivo demonstration of AMG uptake by the newborn kidney cortex. A kinetic analysis of the entry phenomenon in the newborn tubule reveals the presence of two distinct membrane transport systems for AMG, only one of which is present in the adult tubule. All transport of sugar in both newborn and adult tubules was phlorizin-sensitive, but was only partially inhibited in Na+-free buffer. Glucose was shown to inhibit uptake competitively on the shared, high capacity system. Uptake on the high affinity system in the newborn represents 15-20% of the total at physiologic sugar concentrations. It is concluded that active sugar transport is a characteristic of the newborn rat kidney and that the isolated tubule preparation is a more accurate reflection of this phenomenon than is the renal cortical slice.SpeculationThe presence of a unique high affinity glucose transport system in newborn renal tubules in addition to the lower affinity system also found in the adult enables the anatomically immature kidney to efficiently reclaim sugar from the glomerular filtrate and, thus, to prevent loss of calorically valuable nutrients in the promotion of growth.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

摘要:

SummaryLipoprotein lipase activity in lung and heart was studied in fetal (17-22 days of gestation) and newborn rats from the day of birth until 30 days of age. Enzyme activity in epididymal, omental, and parametrial adipose tissue was tested after 18 days of age. Blood triglyceride levels were measured at all ages from 17 daysin uterountil 30 days after birth.The developmental pattern of lipoprotein lipase differed markedly in lung and heart. Although lipoprotein lipase activity was 4 to 5 times higher hi adult rat heart than in lung (30-40 U/g in heart vs. 8-11 U/g in lung), the activity was almost completely absent from fetal heart and was very low during the first 3 days after birth. Lipoprotein lipase reached 60-70% of adult activity at 6 days and remained at that level until 19 days after birth; adult activity levels were reached at 24 days. In the lung, contrary to the heart, lipoprotein lipase activity was high in the fetus (84% of adult activity), decreased immediately after birth to 45% of adult activity at 2 days, and remained at that level up to 15 days after birth. Enzyme activity started to rise again at 15 days and reached adult levels at 21 days of age. Adipose tissue was present in trace amounts before the age of 2 weeks. In the three fat depots tested, lipoprotein lipase activity was 50% lower than in adults between 20 and 30 days after birth. Blood triglyceride levels increased 4- fold between 2 to 10 hr after birth and remained elevated during the first 3 days after birth.SpeculationThe triglyceridemia that starts in the immediate postnatal period and lasts for several days in the rat probably results from the combination of high fat intake and low clearing ability of the extrahepatic tissues.In addition to its role in clearing circulating triglyceride, lipoprotein lipase may play a role in the growth and maturation of individual organs. The present study shows that lipoprotein lipase activity is high in fetal lung during the period of marked surfactant synthesis and suggests that circulating triglyceride-fatty acids are used by the fetal lung for surfactant synthesis.

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1978

数据来源: OVID