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Biomedical subjects

D O Allen

Publications and source records attributed to D O Allen.

At least 55 records · Page 3Linked to original sources
PubMed1973

Evidence for delayed development of the glucagon receptor of adenylate cyclase in the fetal and neonatal rat heart.

The effects, in vivo, of epinephrine, glucagon, and dibutyryl cyclic adenosine 3',5'-monophosphate (cyclic AMP) on the glycogen content of rat heart and liver and, in vitro, upon adenylate cyclase activity in homogenates of rat heart and liver were determined during the latter third of gestation and the neonatal period. Hepatic glycogen was depleted by epinephrine, glucagon, and dibutyryl cyclic adenosine 3',5'-monophosphate, but myocardial glycogen was depleted only by epinephrine and dibutyryl cyclic AMP in the neonates. Hepatic adenylate cyclase activity was augmented by both epinephrine (10(-5) M) and glucagon (10(-5) M), and myocardial cyclase was increased only by epinephrine in tissue obtained from 16, 18, and 20 day fetal rats. Myocardial adenylate cyclase responsiveness to glucagon was present in tissue obtained from rats 4 wk of age and older. It is concluded that in contrast to hepatic adenylate cyclase, myocardial adenylate cyclase in the rat is not responsive to glucagon during gestation and that responsiveness to glucagon and the associated ability of glucagon to deplete myocardial glycogen do not develop until well after birth.

Adenylyl Cyclases↗
PubMed1973

Hormone-stimulated lipolysis in isolated fat cells from "young" and "old" rats.

The biphasic nature of the lipolytic dose-response curve of epinephrine in fat cells from "young" rats (40-45 days) was confirmed. The first phase (Lipolysis I) occurred at concentrations of from 10(-7) m to 3 x 10(-6) m. The second phase (Lipolysis II) occurred at concentrations of from 10(-5) m to 3 x 10(-4) m. Insulin (0.1 mU/ml) abolished Lipolysis I and slightly augmented Lipolysis II. Higher concentrations of insulin (1.0 mU/ml) augmented Lipolysis II even further. These results may help to explain some of the conflicting reports in the literature concerning the effects of insulin on lipolysis. The dose-response curve of epinephrine using fat cells from "old" rats (14-16 months) was monophasic. Based on results with propranolol, K(+)-free media, and insulin, it was concluded that the lipolytic response in tissue from older animals corresponds to Lipolysis II in tissue from younger rats. The lipolytic response to ACTH was greatly reduced in the cells from the older rats, but the response to theophylline was unaltered.

Adipocytes↗
PubMed1972

Effects of dibutyryl cyclic adenosine 3',5'-monophosphate and parathyroid extract on calcium and phosphorus metabolism in hypoparathyroidism and pseudohypoparathyroidism.

It has been proposed previously that the metabolic defect in pseudohypoparathyroidism which accounts for parathyroid hormone unresponsiveness is an absence or abnormal form of the adenyl cyclase system in kidney and presumably in bone. To determine whether there is an associated defect in the response mechanism to cyclic adenosine 3',5'-monophosphate (cyclic AMP), the effects of parathyroid extract (PTE), and dibutyryl cyclic AMP were compared in patients with either surgical hypoparathyroidism or pseudohypoparathyroidism. PTE and dibutyryl cyclic AMP both increased serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in patients with hypoparathyroidism. PTE also increased urinary cyclic AMP in these patients. PTE increased serum and urinary calcium and urinary phosphorus but did not alter serum phosphorus or urinary cyclic AMP in the patients with pseudohypoparathyroidism. Dibutyryl cyclic AMP increased the serum and urinary calcium, lowered the serum phosphorus, and increased urinary phosphorus in all the patients with pseudohypoparathyroidism. The results indicate that (a) dibutyryl cyclic AMP can reproduce the effects of parathyroid hormone on calcium and phosphorus metabolism in man, (b) the response mechanism to cyclic AMP appears to be intact in pseudohypoparathyroidism, and (c) PTE apparently produces some of its characteristic effects on calcium and phosphorus metabolism in pseudohypoparathyroidism in the absence of an increase in urinary cyclic AMP.

Adolescent↗