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Biomedical subjects

R A Sharp

Publications and source records attributed to R A Sharp.

25 records · Page 2Linked to original sources
PubMed1985

Organ culture of isolated rat pancreatic islets with reference to A-cell function.

Investigation of the control of glucagon secretion has suffered from the lack of suitable in vitro models. The present studies were initiated to further validate the use of organ cultured islets for such investigation and to develop methods for obtaining rat islets relatively depleted of B cells. Rat islets maintained in tissue culture for 1 week are shown to respond to glucose, epinephrine, acetylcholine, arginine, and somatostatin in a physiologic manner. High glucose concentration during culture is associated with increased glucagon secretion despite increased insulin secretion. Treatment of rats with diabetogenic agents just prior to islet isolation results in B-cell deterioration during culture and insulin content about 20% normal after 1 week of culture. B-cell depleted islets show no glucagon suppression by glucose despite the presence of insulin.

Acetylcholine↗
PubMed1983

Modification of chemically induced diabetes in rats by vitamin E. Supplementation minimizes and depletion enhances development of diabetes.

Administration of the antioxidant vitamin E to rats, prior to administration of either streptozotocin or alloxan, provided protection against the diabetogenic effect of both these agents. This was demonstrated by their response to a glucose load, their pancreatic insulin content and light microscopy findings. In addition, rats whose antioxidant state was depleted, by being maintained on a vitamin E and selenium-deficient diet, demonstrated increased diabetogenic susceptibility to normally nondiabetogenic doses of streptozotocin. These findings provide indirect support for the suggestion that the chemical agents streptozotocin and alloxan may exert their diabetogenic effect by acting as oxidants or free radical producers.

Alloxan↗
PubMed1980

Protection against streptozotocin-induced diabetes by superoxide dismutase.

Suerpoxide dismutase was administered intravenously to rats 50 min prior to intravenous administration of a diabetogenic dose of streptozotocin. A dose of 45 mg/kg streptozotocin alone produced marked glucose intolerance and a decrease in pancreatic insulin content to less than 10% of control; both of these effects were abolished by prior administration of 105 mu/g of superoxide dismutase. Superoxide dismutase (105 mu/g) administered 50 min before 65 mg/kg intravenous streptozotocin did not prevent the development of diabetes. The fall in pancreatic insulin content seen with streptozotocin alone was, however, partially reversed by superoxide dismutase.

Animals↗