Search

The continuous infusion of glucose (1 mg/kg/min) via the carotid artery in anesthetized dogs produces a biphasic pattern of insulin secretion. The first peak reaches a maximum 3 min after glucose infusion and drops to basal level at 7 min. As long as the glucose infusion persists a slow and mantained increase in insulin level in the pancreaticoduodenal vein can be observed. The same amount of glucose infused in the general circulation via the jugular vein provoked a different pattern of insulin secretion. Cerebral glucose infusion to vagotomized dogs also produced a two phase response to insulin secretion, but the levels reached in the first phase were lower that those observed in the normal dogs. The infusion of glucose, via the jugular vein, in vagotomized dogs, failed to induce any change in plasma insulin levels. Our data suggest that a glucose load to the brain induces pancreatic insulin secretion mediated partially by the vagus nerves. These results are also compatible with the hypothesis that a humoral factor could be involved in the pancreatic response.

The present experiment was performed in the Antartic continent at 64° 53′ S Lat.; 62° 53′ W Long. The following studies were carried out in the Gentoo penguins (Pygocellis papua). A—Pancreatic response to intravenous injection of arginine and phenformin. B—Changes in blood sugar levels, urea, and uric acid induced by the intravenous injection of arginine and phenformin. C—Changes in blood sugar levels elicited by the injection of porcine crystalline insulin. Intravenous injection of arginine raised the plasma immunoreactive insulin (IRI) 5 and 15 min after its administration. Phenformin failed to induce any modification in the circulating level of IRI. Plasma urea and uric acid levels were found to be elevated after arginine injection. The injection of phenformin did not modify the plasma urea level, increased the plasma uric acid values and lowered the blood sugar levels. Crystalline insulin lowered the blood sugar level. The same effect was observed when insulin was injected after 13 days of starvation.

The present experiment was performed in the Antartic continent at 64° 53′ S Lat; 62° 53′ W Long. Gento penguins ( Pygocellis papua ) were studied after 24–48 hr and 6–12 days of starvation. After intravenous injection of glucose (1 g/kg), the blood sugar levels remained elevated for periods up to 10 hr. Starvation did not affect the glucose tolerance curve. The pancreatic function was tested using hipoglycemic agents. Tolbutamide (200 mg/kg) and chlorpropamide (100 mg/kg) did not induce any changes in the blood sugar level. Inmunoreactive serum insulin level was about 40 μU/ml after 24–48 hr of starvation. This value fell to about 10 μU/ml after 12 days of starvation. Intravenous glucose injection was without significant effect in insulin secretion.

In experiments performed at the Almirante Brown Scientific Station (64° 53′ South; 62° 53′ West), arginine induced in penguins significant release of insulin from incubated pieces of pancreas, while glucose acted as stimulus only at very high concentrations. Substances active on the adenyl cyclase system, such as glucagon, theophylline, isoproterenol, and even 3′,5′ cyclic AMP, stimulated insulin release. l -Propranolol inhibited isoproterenol-induced insulin release. Phentolamine, in the doses used, had no effect on either basal or isoproterenol-induced insulin secretion. Ouabain and glibenclamide failed to promote any change in the amount of insulin secreted. The results suggest that (a) in the penguin pancreas arginine rather than glucose may be a prominent stimulus for insulin secretion; (b) the penguin beta cell shows decreased sensitivity to glucose; (c) the adenyl cyclase system plays an important role in the mechanism(s) regulating insulin secretion; (d) under our experimental conditions, adrenergic modulation of insulin release is mediated chiefly through beta receptors.