Calle C, Sanchez-Casas P, Simón M A, Mayor P
Biochem Biophys Res Commun. 1987 May 29;145(1):90-5. doi: 10.1016/0006-291x(87)91291-5.
Evidence for pre-receptor, receptor and post-receptor glucagon defects was investigated in adipocytes from cortisol-treated rats. A decrease in glucagon binding due to a decreased number of receptors was observed. No changes in receptor affinity were detected. Both, the lipolytic response of glucagon and the ability of glucagon to increase basal and theophylline-stimulated cAMP accumulation remained unaltered. Moreover, a hyperglucagonemia accompanied by an increase in glucagon degradation in the serum of cortisol-treated rats was observed. Such alterations could represent a new mechanism by which glucocorticoids exert their biological actions.
在皮质醇处理的大鼠脂肪细胞中研究了受体前、受体和受体后胰高血糖素缺陷的证据。观察到由于受体数量减少导致胰高血糖素结合减少。未检测到受体亲和力的变化。胰高血糖素的脂解反应以及胰高血糖素增加基础和茶碱刺激的环磷酸腺苷(cAMP)积累的能力均未改变。此外,观察到皮质醇处理的大鼠血清中伴有胰高血糖素降解增加的高胰高血糖素血症。这种改变可能代表糖皮质激素发挥其生物学作用的一种新机制。