GROWTH HORMONE AND EXPERIMENTAL DIABETES*

Publisher Website
Google Scholar
Abstract
THE diabetogenic action of purified preparations of the anterior pituitary growth hormone in normal (1, 2, 3) and in partially depancreatized (4, 5) animals is now well attested. Whether or not this effect is produced by growth hormone uncontaminated by other pituitary hormones is still uncertain, and, in the present unsatisfactory state of knowledge concerning the criteria of purity of proteins, it would be unwise to assume that our best preparations of growth hormone are indeed free from physiologically significant amounts of other substances. The possibility that traces of adrenocorticotropin may be present in our preparations of growth hormone and may play a vital role in the etiology of growth-hormone induced diabetes cannot at present be ruled out. Evidence that the secretion of extra insulin by the pancreatic islets is a condition for the exertion of the normal growth-promoting activity of growth hormone in higher animals is circumstantial and perhaps inconclusive, although we nevertheless believe that such is the case. It is, however, clear that some retention of nitrogen can occur under the influence of pituitary extracts in normal animals in circumstances where the secretion of extra insulin cannot take place (3, 6). Such evidence does not contradict the view that a rise in the rate at which insulin is secreted by the pancreas does take place when growth hormone is administered to an animal possessing pancreatic islet tissue. The fact that a fall in blood sugar level may sometimes be encountered as the result of the administration of growth hormone to animals possessing islet tissue (4, 7, 8) suggests the possibility that either the growth hormone acts directly on the islets to stimulate the secretion of insulin or, more probably, the action of growth hormone in antagonizing the peripheral action of insulin may cause insulin to be utilized in the tissues at such an abnormally high rate that the level of insulin in the blood falls. This fall in blood insulin concentration may itself stimulate the secretion of insulin by the pancreatic islets. Such a hypothesis agrees with the fact that the blood sugar level does not rise during the first few days of the daily administration of a diabetogenic growth-promoting anterior pituitary extract to a normal dog or cat, although during this latent period the rate of secretion of insulin by the pancreatic islets may be ten to twenty times the normal value (9).