Taouis M, Derouet M, Chevalier B, Simon J
INRA, Station de Recherches Avicoles, Nouzilly, France.
Gen Comp Endocrinol. 1993 Feb;89(2):167-75. doi: 10.1006/gcen.1993.1020.
The effects of chronic corticosterone treatment (6 mg/kg/day) on insulin sensitivity and on liver and muscle insulin receptors were examined in 5-week-old chickens. The hypoglycemic effect of exogenous insulin was completely abolished within 2 weeks of treatment, suggesting a corticosterone-induced insulin resistance. Hepatic insulin receptor numbers were slightly reduced (P < 0.001) after 2 weeks of treatment. After 1 or 2 weeks, corticosterone treatment significantly reduced liver insulin receptor kinase activity toward the artificial substrate poly(Glu4,Tyr1). Muscle insulin receptor kinase activity was also significantly decreased after 1 week of treatment but this effect was accounted for by a decrease in basal activity. Therefore the corticosterone-induced insulin resistance is accounted for, at least in part, by altered hepatic receptor numbers and kinase activity. The impairment of muscle development involves postreceptor defects.
在5周龄的雏鸡中研究了慢性皮质酮治疗(6毫克/千克/天)对胰岛素敏感性以及肝脏和肌肉胰岛素受体的影响。治疗2周内,外源性胰岛素的降血糖作用完全消失,提示皮质酮诱导的胰岛素抵抗。治疗2周后,肝脏胰岛素受体数量略有减少(P <0.001)。治疗1周或2周后,皮质酮治疗显著降低了肝脏胰岛素受体对人工底物聚(Glu4,Tyr1)的激酶活性。治疗1周后,肌肉胰岛素受体激酶活性也显著降低,但这种作用是由基础活性降低引起的。因此,皮质酮诱导的胰岛素抵抗至少部分是由肝脏受体数量和激酶活性改变所致。肌肉发育受损涉及受体后缺陷。