Ketelslegers J M, Maes M, Maiter D, Thissen J P, Triest S, Underwood L E, Lambert A E
Unité de Diabétologie et Nutrition, Faculté de Médecine, l'Université catholique de Louvain-en-Woluwe.
Bull Mem Acad R Med Belg. 1990;145(1-2):132-41; discussion 141-3.
We investigated the cellular mechanisms responsible for growth hormone (GH) resistance in diabetes and malnutrition in the rat. In insulin-dependent diabetes, a post-receptor defect participates in GH resistance. During fasting, there is a loss of liver GH binding sites. Dietary protein restriction causes a post-receptor defect. This defect can be attributed to the combined effects of decreased liver IGF-I mRNA content and impaired message translation.
我们研究了大鼠糖尿病和营养不良状态下生长激素（GH）抵抗的细胞机制。在胰岛素依赖型糖尿病中，受体后缺陷参与了GH抵抗。禁食期间，肝脏GH结合位点减少。饮食蛋白质限制导致受体后缺陷。这种缺陷可归因于肝脏IGF-I mRNA含量降低和信息翻译受损的联合作用。
