Clinical studies have suggested that excess dietary iodine promotes autoimmune thyroiditis; however, the lack of a suitable animal model has hampered investigation of the phenomenon. In this study, different amounts of potassium iodide were added to the diets of chicken strains known to be genetically susceptible to autoimmune thyroiditis. Administration of iodine during the first 10 weeks of life increased the incidence of the disease, as determined by histology and the measurement of autoantibodies to triiodothyronine, thyroxine, and thyroglobulin. Further support for the relation between iodine and autoimmune thyroiditis was provided by an experiment in which iodine-deficient regimens decreased the incidence of thyroid autoantibodies in a highly susceptible strain. These results suggest that excessive consumption of iodine in the United States may be responsible for the increased incidence of autoimmune thyroiditis.
The effect of TRH on GH secretion was assessed in 13 insulin-dependent diabetics. PRL and TSH responses to TRH were also determined. Glycosylated hemoglobin levels and serial fasting glucose concentrations indicated that all but 1 of the patients had a period of poor diabetic control for several months before the study. Peak PRL and TSH levels after TRH injection in these diabetic patients did not differ significantly from values observed in nondiabetic individuals. Six of the patients responded to TRH with a significant rise in GH levels; basal GH concentrations were also elevated in these patients. Five of the 6 responders and none of the nonresponders had proliferative diabetic retinopathy. The results suggest that diabetics with elevated basal GH levels hyperrespond to TRH, and that nonspecific secretion of GH in response to TRH occurs in some patients with proliferative diabetic retinopathy. Chronic hyperglycemia does not appear to be the critical factor in determining this response.
Incubation of purified rat glomerular basement membrane (GBM) with [14C]-glucose in vitro resulted in the incorporation of [14C] into acid-precipitable radioactivity in a reaction that was time and temperature dependent. Findings with rat lens capsule basement membrane (LCBM), an anatomically distinct but chemically similar extracellular matrix, incubated for varying times at different temperatures with [14C]-glucose at constant specific activity were similar. Nonenzymatic glycosylation of basement membrane, documented by hydroxymethylfurfuraldehyde generation after incubation with unlabeled glucose, increased in proportion to the ambient glucose concentration over a range of 5--100 mM. Acid-precipitable radioactivity also increased in proportion to [14C]-glucose concentration, although this method overestimated glycosylation about 15-fold at 5--20 mM glucose and 50-fold at 50--100 mM glucose. Coupled with recent in vivo studies, these findings indicate that exposure to increased glucose concentration alters the chemistry of glomerular and other basement membranes. Since accumulation of basement membrane characterizes several of the microangiopathic sequelae of diabetes, the role of increased nonenzymatic glycosylation on the structure, function, and metabolism of basement membrane warrants investigation.
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