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Biomedical subjects

L Picon

Publications and source records attributed to L Picon.

At least 91 records · Page 5Linked to original sources
PubMed1980

Postmaturity in the rat: glucose metabolism in the fetus and the neonate.

The present study was designed to investigate glucose metabolism in the postmature fetus and newborn. In the fetus, the decreased hepatic glycogen content together with the decrease by the same percentage of total hepatic glycogen radioactivity from directly injected [6-3H]glucose demonstrate that fetal glycogenolysis occurs during prolonged gestation. Moreover, fetal glycogen synthesis as tested by in vivo [6-3H]glucose incorporation experiments is inhibited. In vivo experiments with [14C]lactate are consistent with gluconeogenesis, being inactive in the postmature fetus as well as in the normal-term fetus. During the first hr after delivery, our in vivo data about conversion of [14C]lactate to glucose show that the gluconeogenic pathway is not functioning in spite of very high phosphoenolpyruvate carboxykinase activity in the postmature. By 3 hr postpartum, the phosphoenolpyruvate carboxykinase activity, the blood lactate level, the percentage of conversion, and the rate of gluconeogenesis are very elevated in the postmatures as compared to the term neonates. By 6 hr postpartum, despite maintained phosphoenolpyruvate carboxykinase activity, gluconeogenic rate becomes very weak in postmatures kept fasting. This is the time characterized by a profound hypoglycemia. In contrast, fed postmature neonates exhibit normal blood glucose levels by 6 and 12 hr postpartum as a result of sustained rate of gluconeogenesis.

Animals↗
PubMed1980

Diabetogenic effect of N-nitrosomethylurea and N-nitrosomethylurethane in the adult rat.

Sodium nitrite and two N-nitroso compounds, N-nitrosomethylurea (NMU) and N-nitrosomethylurethane (NMUT) have been investigated in the adult rat with regard to their in vivo effects on glucose tolerance and insulin response to glucose. Their effects have been compared to the diabetogenic action of streptozotocin (SZ). Glucose challenge (0.5 g/kg) in order to test insulin secretion in vivo gives the same result in the sodium nitrite-treated (25 mg/day during 2 months administered in drinking water) as in the control rats. In the NMU-treated (100 mg/kg i.p.) and in the NMUT-treated (100 mg/kg i.p.) glucose-induced insulin secretion tested 1 or 8 days after drug administration is severely decreased during the second test, especially in the NMUT-treated rats. Rats receiving STZ (35 mg/kg i.v.) exhibit sluggish insulin secretion as soon as the first test. Since in situ formation of nitrites and nitrosamines has been detected in human, one wonders about their role in the aetiology of human diabetes.

Animals↗
PubMed1979

Chemical diabetes in the adult rat as the spontaneous evolution of neonatal diabetes.

Injection of streptozotocin in newborn rats induced a severe diabetic syndrome on day 4 after birth, with acute hyperglycaemia and glycosuria. Over the next 3 weeks spontaneous recovery occurred as attested by normal basal blood glucose and plasma insulin levels. Recovery was, however, incomplete in the adult since a definite impairment in insulin release and glucose disposal was observed. This state was characterized by the following features: 1) a 72% decrease in pancreatic insulin stores without change in pancreatic glucagon stores; 2) a slight but consistent elevation of blood glucose in the fasted and fed basal states and especially of blood glucose 90 min after an IV glucose load (2 g/kg) performed under pentobarbitone anaesthesia; 3) a considerable decline in the glucose-induced insulin release with a decrease in the maximal response. Both early and late phases of insulin release were impaired, as indicated by in vivo glucose infusion experiments. Basal plasma glucagon levels were normal. Over a period of 12 months with a normal laboratory diet no aggravation of the chemical diabetic state was observed. This new experimental syndrome is a potentially interesting model for the study of the influence of environmental factors on the development of overt diabetes.

Aging↗
PubMed1979

Thyroid hormones and adipose tissue development.

The effect of thyroid hormones on the cellularity of the retroperitoneal adipose tissue (R.P.A.T.) was investigated in rats that were 3, 6 and 12 weeks old. Two groups of rats were respectively made hypothyroid by the antithyroid compound propylthiouracil, or hyperthyroid by thyroxine. The number of adipocytes was less in the hypothyroid rats than in the controls; it was higher in the hyperthyroid rats without any concomitant increase in the weight of their R.P.A.T. Moreover, there was no significant correlation between adipose cell number and adipose tissue weight within any group of T4 or control rats. In all groups of rats, the number of adipose cells in the R.P.A.T. was larger in males than in females; the difference was highly significant in 12 week old control rats.

Adipose Tissue↗
PubMed1978

Postmaturity in the rat: phosphorylase, glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities in the fetal liver.

Liver glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities were increased in the postmature rat fetus (23.5 day old) when compared to term rat fetus (21.5 day old). Postmaturity was without effect on liver phosphorylase activity. The three liver enzyme activities were also determined in normal 2 day old neonates. These results are correlated with the mobilisation of fetal liver glycogen occuring during postmaturity in the rat and are discussed in relation to the secretory pattern of the pancreatic hormones.

Animals↗
PubMed1976

Postmaturity in the rat: impairment of insulin, glucagon, and glycogen stores.

Prolonged gestation (2 extra days in utero) was obtained by daily subcutaneous injection of progesterone (2.5 mg) to pregnant rats from day 20.5 post coitum (p.c.) throughout day 22.5 p.c. after reduction of the litter to 6 fetuses on day 14.5 p.c. Exogenous progesterone per se or litter reduction were without effect of fetal pancreas or fetal liver. Plasma insulin, insulin and glucagon in the pancreas, and liver glycogen stores have been systematically measured in postmature animals and in controls during the perinatal period. In 23.5 day-old postmature as compared to 21.5 day-old normal fetuses, the intrauterine mortality was increased (26%), the body weight was increased by 30%, the liver weight was decreased by 20%, the glycogen content of liver was dramatically depleted (1.1 +/- 0.2 mg/g body weight on day 23.5 p.c. against 6.7 +/- 0.3 on day 21.5 p.c.), the plasma insulin was lowered by 63% and the blood glucose level was normal. In postmature neonates during the first day of life the mortality rate was considerable (40%) and a dramatic fall of blood glucose was observed 6 hours after birth. The accumulation of insulin and glucagon in the pancreas, which normally occurs in the two first days after birth, was much lower in the postmature fetuses: in 23.5 day-old fetuses as compared to 2 day-old normal newborns of the same gestational age the insulin content was only 50% and the glucagon content 69%. The deficit of insulin accumulation in the postmature pancreas lasted at least five days. The ability of the endocrine pancreas to recover from this alteration as well shown by the lack of diabetes when the animals were examined three weeks later by a glucose tolerance test. These findings suggest that the drop of plasma insulin is a prime factor in causing the lack of glycogen stores in prolonged fetuses and the impairement of glycogen stores appear to be an important feature of postmaturity, since neonates exhibit, in these conditions, a lethal drop of blood glucose as glycogenolysis operates on very low glycogen stores.

Animals↗