Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Postmaturity in the rat: impairment of insulin, glucagon, and glycogen stores. 98 49

Continuous glucose infusion was used to induced mild hyperglycaemia in unrestrained pregnant rats during the last three days of pregnancy. Control pregnant rats were infused with distilled water. Fetuses were studied after normal or prolonged pregnancy. Fetuses from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a rise in the glucagon/insulin ratio from 6.5 to 67 in fetuses from control rats and from 1.3 to 13 in fetuses from glucose-infused rats. Concurrently in fetuses from control rats, liver phosphoenolpyruvate carboxykinase activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser extent. These results show that both the A and B cells of the rat fetal pancreas are sensitive to chronic glucose stimulation.
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PMID:Hyperglycaemia induced by glucose infusion in the unrestrained pregnant rat during the last three days of gestation: metabolic and hormonal changes in the mother and the fetuses. 704 Jan 46