Mayor P, Calle C
Department of Biochemistry, School of Medicine, Complutense University, Madrid, Spain.
Endocrinol Jpn. 1988 Apr;35(2):207-15. doi: 10.1507/endocrj1954.35.207.
Evidence for pre-receptor, receptor and post-receptor glucagon defects was investigated in adipocytes from streptozotocin-diabetic rats. For this purpose male Wistar rats were injected by cardiac puncture with streptozotocin (65 mg/Kg body-weight) or saline solution and sacrificed after 7 and 15 days of drug administration. Increased glucagon levels and increased glucagon degradation in serum together with a decrease in glucagon binding were found in both groups of diabetic rats. The decrease in glucagon binding was related to a decrease in the number of glucagon receptors/cell rather than to a change in receptor affinity. The lipolytic response of glucagon was increased. However, the ability of glucagon to increase basal or theophylline-stimulated cAMP accumulation in the incubation medium of adipocytes from diabetic rats was decreased. Such alterations could represent a counter-regulatory mechanism of the hyperglucagonemia detected in streptozotocin-diabetic rats.
在链脲佐菌素诱导的糖尿病大鼠脂肪细胞中,研究了受体前、受体和受体后胰高血糖素缺陷的证据。为此,通过心脏穿刺给雄性Wistar大鼠注射链脲佐菌素(65mg/kg体重)或生理盐水,并在给药7天和15天后处死。两组糖尿病大鼠均出现血清中胰高血糖素水平升高、胰高血糖素降解增加以及胰高血糖素结合减少。胰高血糖素结合减少与胰高血糖素受体/细胞数量减少有关,而非受体亲和力改变。胰高血糖素的脂解反应增强。然而,胰高血糖素增加糖尿病大鼠脂肪细胞孵育培养基中基础或茶碱刺激的环磷酸腺苷(cAMP)积累的能力下降。这些改变可能代表了链脲佐菌素诱导的糖尿病大鼠中检测到的高胰高血糖素血症的一种反调节机制。