摘要:

We have investigated the respective roles of insulin and glucagon in the initiation of hepatic glycogen degradation during the early postnatal period in rats, with special regard on the inhibitory effect of insulin on this process. Pregnant rats were rendered either slightly (8.5 mM) or highly hyperglycemic (22 mM) by infusing glucose during the last week of pregnancy. Fasted, newborn rats were studied from delivery to 16 h postpartum. At birth, newborns from slightly hyperglycemic rats showed higher glycemia and insulinemia and lower plasma glucagonemia compared with controls. Newborns from highly hyperglycemic rats were still more hyperglycemic and exhibited low plasma glucagon concentrations, but they were not hyperinsulinemic. In control newborns, hepatic glycogen breakdown was triggered by 2 h after delivery. By contrast, hyperglycemic-hyperinsulinemic newborns (newborns from slightly hyperglycemic rats) were unable to mobilize liver glycogen before 8–10 h after delivery. In hyperglycemicnormoinsulinemic newborns (newborns from highly hyperglycemic rats), hepatic glycogen concentration significantly started to decline 2 h after delivery and was no longer different from controls at 8 h. Anti-insulin serum injection at delivery promoted a prompt decrease in liver glycogen stores in controls as well as in newborns from slightly hyperglycemic rats. Phosphorylase a/synthase a ratio rose rapidly after delivery in controls and in newborns from highly hyperglycemic rats (maximum 4 h), whereas in newborns from slightly hyperglycemic rats, it rose much more slowly than in the two other groups (maximum 16 h). These data suggest that, in newborns from hyperglycemic mothers, hyperinsulinemia during late fetal and early neonatal life is the main factor preventing postnatal hepatic glycogenolysis.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Lactate concentration and oxygen content were measured in 21 normal (AGA) and 34 intrauterine growth-retarded (IUGR) infants at the time of elective cesarean section. Maternal lactate and umbilical arterial and venous lactate concentrations were significantly higher in IUGR infants compared with AGA infants. However, when IUGR patients were subdivided according to pulsatility index (PI) measurements of the umbilical artery, no differences were detected between AGA and IUGR patients with PI <4 SD, whereas IUGR patients with PI >4 SD had higher lactate concentrations in maternal arterial blood and umbilical arterial and venous blood from both other groups. There was a significant inverse linear relationship between umbilical arterial lactate concentration and umbilical venoarterial differences for both lactate concentrations and for lactate/oxygen quotients. These relationships were significantly different in IUGR fetuses with PI >4 SD compared with AGA and IUGR fetuses with PI <4 SD. AGA and IUGR fetuses with PI <4 SD have arterial lactate concentrations <2 mM even at low oxygen concentrations (O2content <2 mM, O2saturations <20%). At comparable levels of oxygenation, IUGR fetuses with PI >4 SD have a marked lactacidemia. The data suggest that coupling Doppler assessment of flow velocimetry with biochemical analyses of fetal blood can be useful in identifying a subset of IUGR human fetuses at risk of intrauterine hypoxia.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

A child presented in early childhood with episodes of coma and hypoglycemia and a rapidly evolutive myopathy and cardiomyopathy leading to death at 9 mo of age. Ketosis was decreased (blood β-hydroxybutyrate: 0.07 mmol/L) despite normal plasma levels of fatty acids (0.81 mmol/L). The patient's urine contained excessive amounts of the C6to C10dicarboxylic acids present in almost all defects of fatty acid mitochondrial oxidation. More specifically, gas chromatography-mass spectrometry identified an accumulation of medium- and long-chain (C8to C14) 3-hydroxy-dicarboxylic acids, suggesting a defect of the mitochondrial enzyme that normally dehydrogenates these 3-hydroxyacyl-CoA esters. Biochemical studies in the patient's cultured fibroblasts confirmed the impairment of medium- and long-chain fatty acid oxidation, and allowed the recognition of the deficiency of long-chain 3-hydroxyacyl- CoA dehydrogenase. The activities of long-, medium-, and short-chain acyl-CoA dehydrogenases and 3-ketoacyl- CoA thiolase were normal. These results describe a disorder of fatty acid metabolism that affects the liver, skeletal muscles, and myocardium. It is important to point out that long-chain 3-hydroxyacyl-CoA deficiency shares many clinical similarities with systemic carnitine deficiency, as well as with carnitine-palmityl-CoA transferase and longchain acyl-CoA dehydrogenase deficiencies. The differential diagnosis of this disease relies on the demonstration of long-chain urinary dicarboxylic acids with a hydroxyl group in 3-position and the study of the enzyme activity in cultured fibroblasts.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The bicarbonate transport rate in neonatal rabbit juxtamedullary proximal convoluted tubules (JMPCT) is lower than that in adults. The reduced rate of transport could be due to a decrease in active bicarbonate transport or an increase in the passive permeability of the tubule to bicarbonate. The present invitromicroperfusion study directly measured the bicarbonate permeability of neonatal and adult JMPCT. Bicarbonate permeability was measured at both slow and fast perfusion rates to simulate the neonatal and adult proximal tubule flow rates, respectively. At 38°C in tubules perfused at 3 nL/min, bicarbonate permeability was 0.29 ±0.11 × 10−5cm/s in neonates and 1.70 ± 0.49 x 10−5cm/s in adult PCT (p< 0.05). At a perfusion rate of 10 nL/min, bicarbonate permeability was 0.11 ± 0.27 x 10−5cm/s in neonatal PCT and 2.31 ± 0.15 × 10−5cm/s in adult PCT (p< 0.05). These results demonstrate that bicarbonate permeability in neonatal JMPCT is significantly lower than that in adult JMPCT. Thus, the lower rate of bicarbonate transport in neonatal PCT is entirely due to a lower rate of active bicarbonate transport.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Murine hybridoma antibodies directed against the capsule and O-side chain determinants of theEscherichia colistrain Bort (018ac:Kl:H7) were evaluated for their ability to enhance bactericidal activity of cord blood against KlE. colistrains possessing O antigens common in neonatalE. coliinfection,i.e. 018, 07, and 01. The antibodies to the Kl capsule and O-side chain efficiently enhanced cord polymorphonuclear leukocyte-mediated killing of Kl encapsulatedE. colistrain possessing a homologous O antigen, but the IgM antibody to the Kl capsule exhibited approximately 10-fold greater activity than did the IgG3 antibody to O-side chain (weight basis). Both antibodies required complement for their opsonic activities. Our findings indicate that antibodies directed against the capsule and O-lipopolysaccharides are able restore the opsonic activity of cord blood against KlE. coli, suggesting that these antibodies may be useful in the prevention and therapy of neonatal.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID