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Analysis of insulin responses of obese prediabetic and diabetic Zucker diabetic fatty (ZDF) rats to glucose and to the glucose metabolites, D-glyceraldehyde and monomethyl succinate, help determine the defects associated with loss of the glucose transporter GLUT-2 in beta-cells of non insulin-dependent diabetic obese rats. Diabetic ZDF rats show impaired insulin responses to glyceradehyde, monomethyl succinate and glucose. The impaired responses are greatest for glucose and lowest for monomethyl succinate, confirming the occurrence of defects at multiple sites in glucose metabolism.

Patients with certain types of autoimmune thyroid diseases may recover spontaneously if their immune system stops producing antibodies against the hormone thyrotropin, which stimulates the thyroid gland. The production of thyrotropin-blocking antibodies can cause hypothyroidism in some of these patients. A study of 172 hypothyroid patients with goitrous autoimmune thyroiditis found that nine percent had thyrotropin-blocking antibodies. Of 64 hypothyroid patients with atrophic autoimmune thyroiditis, 25% had thyrotropin-blocking antibodies. Twenty-one of the patients with thyrotropin-blocking antibodies were treated with the drug levothyroxine to return their thyrotropin levels to normal. Production of thyrotropin-blocking antibodies stopped in 15 of these patients. These 15 patients stopped taking levothyroxine, and six had not become hypothyroid after two years. The other nine became hypothyroid within three months. Thyrotropin-blocking antibodies may be one of the causes of hypothyroidism, and production of these antibodies may spontaneously stop in some patients.

Cushing's syndrome refers to a condition in which the adrenal gland (two glands located just above the kidneys) secretes excess glucocorticoids, one of its products. These hormones have many effects, some of which target the thyroid gland. The development of autoimmune thyroid disease (in which the immune system attempts to destroy its own tissues) was noted in three patients who developed Cushing's syndrome as a result of a tumor of the adrenal gland. Treatment consisted of removal of the affected gland (unilateral adrenalectomy). Twenty-one additional adrenalectomized patients with the same initial diagnosis did not develop signs of abnormal thyroid function. To learn more about a possible relationship between autoimmune thyroid disease and the effects of adrenalectomy, differences between the patients who did and did not develop autoimmune disease are explored. In all patients, signs of Cushing's syndrome disappeared after adrenalectomy. The thyroid dysfunctions of the three patients with autoimmune thyroid disease are described. One had transient hyperthyroidism (excess thyroid function); another, hypothyroidism (deficient thyroid function); the third developed hyperthyroidism and, then, hypothyroidism. Both hyperthyroid patients probably developed thyroiditis, or inflammation of the thyroid gland. It is possible that the (Cushing syndrome-related) oversecretion of glucocorticoids, which suppress the immune response, can protect patients with thyroid autoantibodies (antibodies to their own body's proteins). When the adrenal tumor is removed, the autoimmune process is free to develop. Another possible cause for thyroid abnormalities in these patients is the iodine exposure associated with certain diagnostic procedures. Patients with adrenal tumors who develop Cushing's syndrome should have their thyroid function monitored. (Consumer Summary produced by Reliance Medical Information, Inc.)

The temporal profiles of insulin secretion by isolated pancreatic islets of male Wistar rats with various ages up to 1- year-old were studied using high glucose, potassium (K) depolarization, and arginine as secretagogues. In the islets of 6-month-old rats, the onset and peak of glucose-induced first phase of insulin release were delayed for I min compared to those of 7-week-old rats. The onset and peak were further delayed for 1 min in the islets of 1-year-old rats. The onset of glucose-induced second phase of insulin secretion, and the onset and peak of K depolarization- and arginine-induced insulin release were not delayed in the islets of 6-month and 1-year-old rats. Glucose-stimulated increase in cytosolic free calcium ([Ca]) seemed not delayed in the islets of 1-year-old rats. We conclude that the first phase of glucose-induced insulin release by the islets is selectively delayed as rat ages. It was suggested that the defect lies distal to the elevation of [Ca]. [ABSTRACT FROM PUBLISHER]