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The relation of the thyroid to carbohydrate metabolism has often been commented upon, von Noorden having described, many years ago, what he termed thyroid diabetes. The more recent investigations initiated by Jacobsen (1), and more fully developed by others (2), have emphasized this relation still further. As is well known the work of Jacobsen and others has shown that the ingestion of considerable amounts of glucose is followed by a temporary hyperglycemia. It is generally accepted that when, in the course of this hyperglycemia, the concentration of the blood sugar rises above 185 mgm. per 100 c.c. of blood, in the majority of cases sugar appears in the urine. McCasky (3), who investigated this phase of metabolism in some thirty odd cases of exophthalmic goitre, was unable to demonstrate a specific curve of sugar tolerance in the blood during the disease, although, in common with others, he noted that there was a hyperglycemia even before the administration of glucose. Janney and Isaacson (4), found that the complete extirpation of the thyroid, in dogs, was followed by absence of hyperglycemia when large amounts of glucose were administered. Theories attempting to explain the mechanism of sugar mobilization based on the data at present available are all unsafe, since no theory as yet advanced is sound enough to withstand the application of facts already demonstrated but disregarded in the formulation of any given theory. It may perhaps be permissible to state here that the question of glycemia and the glycemic reaction which follows either the ingestion of large amounts of glucose or the subcutaneous injection of a variety of organic and inorganic substances has a twofold significance: one directly concerned with metabolism; the other associated with the processes of immunity. These phases are considered in other publications (5).
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G. L. Rohdenburg (1920) studied this question.
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