Caro J F, Cecchin F, Folli F, Marchini C, Sinha M K
Department of Medicine, East Carolina University School of Medicine, Greenville, North Carolina.
Horm Metab Res. 1988 Jun;20(6):327-32. doi: 10.1055/s-2007-1010828.
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 alpha-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 decreased by T3 without altering its insulin responsiveness. These results demonstrate the heterogeneity of T3's effects at the postinsulin binding level in the liver.
体内研究表明，肝脏是甲状腺功能亢进症中胰岛素抵抗的主要部位。为了进一步研究甲状腺激素在肝脏中的作用，我们在有和没有1 ng/ml和5 ng/ml三碘甲状腺原氨酸（T3）的情况下，将大鼠原代肝细胞培养物孵育20小时。在不影响基础活性的情况下，5 ng/ml的T3降低了胰岛素刺激（1×10^(-7) M）的脂质合成，但不影响胰岛素刺激的α-氨基异丁酸摄取。通过亲和标记法测定，在125I胰岛素结合、降解、内化或胰岛素受体结构没有任何异常的情况下发生了这些变化。然而，以Glu4:Tyrl作为磷酸受体的基础胰岛素受体激酶活性被T3降低，而不改变其胰岛素反应性。这些结果证明了T3在肝脏胰岛素结合后水平上作用的异质性。
