We have identified a non-insulin-dependent diabetic patient with fasting hyperinsulinemia (90 ,uU/ml), an elevated insulin:C-peptide molar ratio (1.68; normal, 0.05-0.20

No abstract

A 47-yr-old woman who had previously received methimazole (MMI) treatment for hyperthyroidism was found to have glucagon binding autoantibodies in plasma. She had never received glucagon. The binding substances were detected in plasma at the time of a glucagon RIA. [125I]Glucagon binding was inhibited only by porcine glucagon and porcine glicentin, and dissociated at acid pH. The substances proved to be glucagon binding antibodies (immunoglobulin G, L-chain K-type), as determined by ammonium sulfate and radioprecipitation. There were no clinical manifestations related the presence of these autoantibodies. In a survey of 91 patients with thyroid disease, 3 patients whose plasma bound [125I]glucagon were identified among 41 with hyperthyroidism who were receiving MMI treatment. Such binding was not found in plasma from untreated hyperthyroid patients, those receiving propylthiouracil or those with chronic thyroiditis. These findings suggest that the development of glucagon antibodies in hyperthyroidism may be associated with MMI treatment.

Summary.Adult male mice infected with the M variant of encephalomyocarditis virus develop hyperglycaemia acutely as a consequence of B cell injury. The severity of the metabolic disease is variable and many animals become normogtycaemic during convalescence. The islets of Langerhans of these mice exhibit minor structural changes, but there are no significant abnormalities of insulin and glucagon secretion. In contrast, animals with persistent hyperglycaemia exhibit striking morphological alterations in the islets. The A cell mass is prominent, whereas B cells are reduced in number and exhibit striking cytological features. These changes are associated with both hypoinsulinaemia and hyperglucagonaemia.