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A simple and reliable radioimmunoassay of triiodothyronine (T3) using polyethylene glycol 6000 (PEG) to separate free from bound ligands is described. With an increase in concentration of PEG added, the percentage of precipitated bound 125I-T3 rose gradually, reaching a plateau at a final concentration of 12.5%. The addition of human γ-globulin at a final concentration of 0.5mg/ml was required for the precipitation of bound ligands. Time lapse after the addition of PEG and γ-globulin did not affect the precipitation of labeled hormones. The minimal detectable quantity by this method is 12.5ng/dl. Determination of serum T3 by this method gave satisfactorily small interassay and intraassay variations. The PEG method is easy, inexpensive and reliable, especially when a large number of samples are assayed. By using this method, we studied T3 concentration of 12 patients with obesity, 15 patients with anorexia nervosa, and 4 treated patients with anorexia nervosa. The mean plasma T3 concentration in 12 normal control subjects was 129.0±9.1ng/dl, while the plasma T3 levels in patients with obesity, anorexia nervosa, and treated anorexia nervosa were 138.2±5.6, 68.5±0.3, and 81.3±16.2ng/dl, respectively. Plasma T3 in patients with anorexia nervosa was significantly lower than those in obese subjects.

Insulin-dependent diabetes mellitus is frequently associated with organ-specific autoimmune diseases and/or high titers of organ-specific autoantibodies. The effects of thyroid autoantibodies on islet-cell function were examined in the present study. Islet cell surface antibody (ICSAb) was detected in sera from 6 of 40 patients with autoimmune thyroid disease (AITD) who were positive for thyroid microsomal autoantibodies (TMA). Furthermore, all of the ICSAb-positive patients had high TMA titers. In vitro study using isolated rat pancreatic islets revealed that TMA positive sera significantly suppressed glucose-induced insulin release. Only one of 19 (5%) AITD patients showed complement-dependent antibody-mediated cytotoxicity and only one of 6 AITD patients (17%) was positive for antibody-dependent cellular cytotoxicity. These results suggest that TMA has an effect on an antigen of the islet cell membrane in which insulin releasing mechanism might be involved.

Fasting plasma gastrin levels measured by radioimmunoassay were found to be elevated in patients with hyperthyroidism. The intravenous injection of arginine caused an increase of plasma gastrin in hyperthyroid patients as in normal subjects. The elevated gastrin level in patients with hyperthyroidism was significantly lowered after the thyroid function was normalized by treatment.

To investigate the role of the β-adrenergic mechanism in the hypergastrinemia of hyperthyroidism, either a β-adrenergic blocking agent or a β-adrenergic stimulating agentwas administered to patients with hyperthyroidism, to patients with atrophic gastritis, and to normal subjects. Compared to normals, fasting plasma levels of gastrin were elevated in patients with hyperthyroidism and atrophic gastritis [87 ± 4 us. 306 ± 45 or 249 ± 37 pg/ml (mean ± SE); P < 0.01]. After propranolol infusion (20 mg over 60 min), plasma gastrin levels significantlydecreased in hyperthyroid patients to 147 ± 25 pg/ml (P < 0.01). Similarly, in patients with atrophic gastritis and in normal subjects, propranolol infusion was accompanied by a decrease in plasma gastrin levels to 195 ± 34 and 70 ± 5 pg/ml, respectively(P < 0.05). However, the mean maximum percent decrement of plasma gastrin from the basal levels was 2- to 3-fold greater in hyperthyroid patients than in patients with atrophic gastritis or in normal subjects (P < ...

Intravenous infusion of 30 gm. of L-arginine over a period of 45 minutes elicited a biphasic insulin response and a moderate blood glucose rise in normal subjects. In patients with hyperthyroidism, both insulin peaks, especially the second one, were low, with virtual absence of the blood glucose response. A single intravenous injection of 4 gm. of arginine provoked similar uniphasic plasma insulin responses in both normal subjects and hyperthyroid patients. Pretreatment with either glucose or xylitol almost completely restored the biphasic insulin response to arginine in patients with hyperthyroidism, whereas pretreatment with aminophylline only partially improved the insulin response. Combined administration of a small amount of glucose (2.25 mg./kg./min.) with arginine also restored the normal second-phase insulin release, with blood glucose rises similar to those in normal subjects given arginine alone. It is concluded that the plasma insulin response to arginine is impaired, especially in its second phase, in patients with hyperthyroidism due to the absence of a blood glucose rise. The second phase of arginine-induced insulin release seems more dependent on glucose than the first phase.