The juvenile diabetic has a serious loss of pancreatic β-cell mass1 and, consequently, a considerable reduction in circulating insulin. The possible role of insulin antagonists in the hyperglycemia of diabetes has been an issue difficult to lay to rest. In recent years, the hypothesis that glucose nonsuppression of normoglucagonemia or hyperglucagonemia is an essential and important component of diabetes is one that has gained considerable momentum.2 This view has been greatly strengthened by observations that somatostatin (somatotrophin release-inhibiting factor), when administered intravenously to normal and diabetic subjects, both induces a fall in glucagon levels and lowers blood glucose concentration. Specifically, somatostatin has been shown to delay the onset of ketoacidosis in diabetic patients subjected to insulin withdrawal.3,4 All of these evidences notwithstanding, the primary role of insulin in glucose regulation would appear to have been firmly reestablished by the demonstration that pharmacologically induced glucagonemia of some three to
MACLAREN NK, CORNBLATH M. How Much Insulin? Am J Dis Child. 1976;130(12):1307–1308. doi:10.1001/archpedi.1976.02120130013002
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