Raheja K L, Linscheer W G, Coulson R, Wentworth S, Fineberg S E
Horm Metab Res. 1980 Feb;12(2):51-5. doi: 10.1055/s-2007-996199.
The role of endogenous glucagon and insulin on the hepatic glycogen and triglyceride storage syndrome in propylthiouracil (PTU)-induced hypothyroidism was investigated in the chick. PTU feeding in the diet resulted in a progressive increase in liver glycogen concentration associated with a concomitant decrease in hepatic glucose-6-phosphatase (G-6-Pase) activity. Plasma glucagon level was significantly decreased and insulin significantly increased after two days of PTU administration. These enzyme and hormone changes were associated with a significant increase in hepatic glucose-6-phosphate (G-6-P) and a decrease in cyclic AMP levels. Although our results do not directly prove, the data does suggest that the hepatic glycogen storage syndrome observed in the PTU-induced hypothyroidism in the chick is mediated through changes in pancreatic glucagon and insulin secretion. The extent of glycogen accumulation was inversely related to G-6-Pase which is a rate limiting glycogenolytic enzyme. A significant increase in the plasma insulin/glucagon ratio, along with a significant decrease in the hepatic cyclic AMP concentration, could most likely also account for the excessive hepatic triglyceride accumulation in the PTU-treated chicks.
在雏鸡中研究了内源性胰高血糖素和胰岛素对丙硫氧嘧啶（PTU）诱导的甲状腺功能减退症中肝糖原和甘油三酯储存综合征的作用。饮食中添加PTU会导致肝糖原浓度逐渐升高，同时肝葡萄糖-6-磷酸酶（G-6-Pase）活性随之降低。给予PTU两天后，血浆胰高血糖素水平显著降低，胰岛素水平显著升高。这些酶和激素的变化与肝葡萄糖-6-磷酸（G-6-P）显著增加和环磷酸腺苷水平降低有关。虽然我们的结果没有直接证明，但数据确实表明，雏鸡PTU诱导的甲状腺功能减退症中观察到的肝糖原储存综合征是通过胰腺胰高血糖素和胰岛素分泌的变化介导的。糖原积累的程度与作为糖原分解限速酶的G-6-Pase呈负相关。血浆胰岛素/胰高血糖素比值显著增加，同时肝环磷酸腺苷浓度显著降低，这很可能也是PTU处理的雏鸡肝甘油三酯过度积累的原因。
