Prolonged administration of thyroid does not produce diabetes in dogs with an intact pancreas. It does produce it in dogs with only a fragment of 2.5-3 gm. pancreas left by a subtotal pan-createctomy, but with normal blood sugar. Previous treatment with anterohypophysis or thyroid sensitizes these animals to the diabetogenic action of thyroid. Diabetes so produced may be observed either only during the thyroid feeding (thyroid diabetes), or it may persist permanently after stopping the treatment (metathyroid diabetes). In both cases the [beta] cells of the islets are damaged, reversibly in the first, permanently in the second. Insulin secretion stops as is shown by expts. in which the pancreas was grafted into the necks of pancreatectomized dogs. Insulin protects the islets during the 1st stages; later it is no longer efficient. Metathyroid diabetes can be obtained after removal of the gonads, thyroids and adrenal medulla. It could not be obtained in hypophysectomized and adrenalec-tomized dogs, because they died in hypoglycemia when given thyroid. Thyroid feeding increases the severity of slight or advanced diabetes; symptoms are exacerbated (diuresis, ketosis, loss of body wt., etc.) and the progress of the disease is accelerated, shortening survival. Metathyroid diabetes has the same characteristic as pancreatic diabetes: hyperglycemia, glycosuria, ketonuria, fatty liver, increase in protein catabolism, high basal metabolism, the same glucose tolerance curve, sensitiveness to insulin. Hepatectomy produces a fall in blood sugar to hypoglycemic level. In dogs, thyroidectomy does not modify diabetes produced by total pancreatectomy. nor Sandmeyer''s, meta-hypophyseal and metathyroid diabetes.