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갑상선 기능항진증에서 인슐린 분비 및 적혈구 인슐린 수용체에 관한 연구
나우균(Woo Kyun Na),김극배(Guk Bae Kim),유명희(Myung Hi Yoo),윤석중(Seuk Joong Yeon) 대한내과학회 1987 대한내과학회지 Vol.33 No.3
N/A Impaired glucose tolerance is well recognized in hyperthyroidism. To investigate the mechanism of glucose intolerance in hyperthyroidism, we performed IV GTT and erythrocyte insulin receptor assay in 7 normal control, 16 thyrotoxic patients and 6 euthyroid patients after antithyroid medication. The glucose decay constant K was decreaaed (K<1.0) in 31% (5/16) of thyrotoxic patients. Insulin secretion at the 1st phase during IV GTT was inereased in thyrotoxic patients compared with normal control (Area under the curve, 761±196 vs 322±49 μU/ml min p<0.05), but 2nd phase insulin secretion showed no significant difference. 125 I-insulin max. specific binding percent of the erythrocyte showed no significant difference in throtoxic patients compared with normal control (p>0.05). Thyrotoxic patients were divided into two groups: group I (n=11) who showed impaired glucose tolerance (K>1.0) and group II (n=5) who showed impaired glucose tolerance (K < 1.0) during IV GTT. 1st phase insulin secretion was increased in group I compared with group II patients (AUC 941±251 vs 310±132 μU/ml min, p<0. 05), while 2nd phase insulin release showed no significant difference. 125 I-insulin max. specific binding percent of erythrocytes showed no significant difference in group I compared with group II (9.80±0.75/o vs 10.40±0.77%, p>0.05). In 5 euthyroid patients on antithyroid medication, insulin secretion & erythrocyte insulin receptor assay showed no significant change after treatment. In conclusion, Ist phase insulin secretion was increased and erythrocyte insulin receptor assay was normal in thyrotoxic patients, suggesting that pheripheral postreceptor defect or hepatic insulin resistance may be responsible for the glucose intolerance of hyperthyroidism.
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