In vivo studies have demonstrated that the liver is the main site of insulin resistance in hyperthyroidism. To further investigate the effect of thyroid hormone in the liver, we have incubated primary cultures of rat hepatocytes in the presence and absence of triiodothyronine (T3) 1 ng/ml and 5 ng/ml for 20 hr. Without affecting basal activity, T3 5 ng/ml decreased insulin-stimulated (1 x 10-7 M) lipid synthesis but not insulin-stimulated α-aminoisobutyric acid uptake. These changes occur in the absence of any abnormalities in 125I-insulin binding, degradation, internalization or insulin receptors structure as determined by affinity-labeling methods. However, basal insulin receptor kinase activity using Glu4: Tyrl as phospho-acceptor was decreaed by T3 without altering its insulin responsiveness. These results demonstrate the heterogeneity of T3's effects at the postinsulin binding level in the liver.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical