Thompson C S, Sykes R M, Muddle J, Dashwood M R
Department of Physiology, Royal Free Hospital School of Medicine, London.
J Endocrinol. 1991 Jan;128(1):85-9. doi: 10.1677/joe.0.1280085.
In-vitro autoradiography was used to demonstrate the regional distribution of 12I-labelled insulin-binding sites in the liver, kidney and heart of normal rats and rats made diabetic with streptozotocin. The distribution of insulin-binding sites in the liver of control rats was uniformly high, while in the kidney of control rats there was weak 125I-labelled insulin binding in the medulla and dense binding in the cortex. In the hearts of control rats a high density of 125I-labelled insulin-binding sites was evident both in the atrial and ventricular muscle. Non-ketotic diabetes mellitus caused a marked increase in 125I-labelled insulin-binding sites in both the liver and kidney with the former tissue exhibiting a time-dependent (7 to 62 days) increase. There was no apparent effect of diabetes on insulin-binding sites in the heart. Since experimental diabetes causes (1) a decrease in circulating insulin concentration and (2) impaired insulin action at many target tissues, the increase in 125I-labelled insulin-binding sites observed in the present study may represent a compensatory 'up regulation' of insulin receptors.
采用体外放射自显影技术,以显示正常大鼠以及用链脲佐菌素诱导制成的糖尿病大鼠肝脏、肾脏和心脏中¹²⁵I标记的胰岛素结合位点的区域分布。对照大鼠肝脏中胰岛素结合位点的分布普遍较高,而对照大鼠肾脏中,髓质有较弱的¹²⁵I标记胰岛素结合,皮质则有密集结合。在对照大鼠心脏中,心房和心室肌中¹²⁵I标记的胰岛素结合位点密度均很高。非酮症糖尿病导致肝脏和肾脏中¹²⁵I标记的胰岛素结合位点显著增加,肝脏组织呈现出时间依赖性(7至62天)增加。糖尿病对心脏中的胰岛素结合位点没有明显影响。由于实验性糖尿病导致(1)循环胰岛素浓度降低,以及(2)许多靶组织的胰岛素作用受损,因此本研究中观察到的¹²⁵I标记胰岛素结合位点增加可能代表胰岛素受体的一种代偿性“上调”。