Baxter R C, Bryson J M, Turtle J R
Endocrinology. 1980 Oct;107(4):1176-81. doi: 10.1210/endo-107-4-1176.
Somatogenic (i.e. GH) receptors have been studied on liver microsomal membranes from male and female rats. Tracer bovine GH was displaced from its binding sites by GHs of various species, but was displaced only weakly by PRLs. Specific bovine GH binding was 3.5-fold higher to female rat liver membranes than to membranes from males. Streptozotocin-induced diabetes significantly reduced binding, by 80% in females and 50% in males, while insulin therapy to normalize weight gain reversed the decrease in binding. Competitive binding curves were consistent with two independent classes of binding site: low affinity sites with K equal to 0.5 nm-1 in both sexes, and high affinity sites with K equal to 12.1 nm-1 in males and 21.4 nm-1 in females (P less than 0.001). The addition of excess ovine PRL caused a substantial loss of high affinity binding with little loss in the low affinity region, suggesting a weak somatogenic role for ovine PRL. In diabetic animals, low affinity sites were unchanged from normal, while high affinity sites were decreased in number, with no change in affinity, and restored on insulin therapy. Serum immunoreactive rat GH levels were the same in normal and diabetic, male and female animals. These studies suggest that the apparent hepatic resistance to GH seen in diabetes when liver somatomedin release is low despite normal serum GH might be explained by the loss of GH receptors in this condition.
已对雄性和雌性大鼠肝微粒体膜上的躯体性（即生长激素）受体进行了研究。示踪牛生长激素被各种物种的生长激素从其结合位点上置换下来，但仅被催乳素微弱置换。牛生长激素与雌性大鼠肝膜的特异性结合比与雄性大鼠肝膜的特异性结合高3.5倍。链脲佐菌素诱导的糖尿病显著降低了结合，雌性降低80%，雄性降低50%，而使体重增加正常化的胰岛素治疗逆转了结合的减少。竞争性结合曲线与两类独立的结合位点一致：两性中亲和力低的位点，其K等于0.5nm-1，以及雄性中亲和力高的位点，其K等于12.1nm-1，雌性中为21.4nm-1（P小于0.001）。添加过量绵羊催乳素导致高亲和力结合大量丧失，而低亲和力区域丧失很少，这表明绵羊催乳素的躯体生成作用较弱。在糖尿病动物中，低亲和力位点与正常动物无异，而高亲和力位点数量减少，亲和力无变化，胰岛素治疗后恢复。正常和糖尿病的雄性和雌性动物血清中免疫反应性大鼠生长激素水平相同。这些研究表明，在糖尿病中，尽管血清生长激素正常，但当肝脏生长调节素释放较低时出现的明显肝脏对生长激素的抵抗，可能是由于这种情况下生长激素受体的丧失所致。
