Pagano G, Cassader M, Lenti G
Acta Diabetol Lat. 1977 May-Aug;14(3-4):164-9. doi: 10.1007/BF02581404.
We have measured insulin binding to human adipocytes isolated from subcutaneous adipose tissue removed during surgery in normal and insulin-independent diabetics. Collagenase digestion, 125I-monoiodoinsulin and Scatchard's plot were employed to analyze the results. Different kinetic patterns emerged together with differences in the dissociation constant and receptor numbers: in normal subjects K1 was 4 X 10(-9) moles/1 and K20.5 X 10(-8) moles/1, and in diabetic subjects K1 was 2.24 X 10(-9) moles/1 and K2 0.52 X 10 10(-8) moles/1; the two classes of receptors were 100,000 and 300,000 per cell in normals and 50,000 and 180,000 in diabetics. It was clear that even slight diabetes leads to receptor deficiency in adipocytes, though it could not be determined whether this a primary, perhaps genetic, defect or secondary to antibody damage, as suggested by some workers. Feed-back between circulating insulin and specific receptor availability in cells is another possibility.
我们测定了胰岛素与从正常人和非胰岛素依赖型糖尿病患者手术中切除的皮下脂肪组织分离出的人脂肪细胞的结合情况。采用胶原酶消化、125I-单碘胰岛素和斯卡查德作图法分析结果。出现了不同的动力学模式以及解离常数和受体数量的差异：正常受试者中，K1为4×10^(-9)摩尔/升，K2为0.5×10^(-8)摩尔/升；糖尿病受试者中，K1为2.24×10^(-9)摩尔/升，K2为0.52×10^(-8)摩尔/升；正常情况下每细胞两类受体分别为100,000和300,000，糖尿病患者中为50,000和180,000。很明显，即使是轻度糖尿病也会导致脂肪细胞受体缺乏，不过正如一些研究者所指出的，无法确定这是原发性的，可能是遗传性缺陷，还是继发于抗体损伤。循环胰岛素与细胞中特定受体可用性之间的反馈是另一种可能性。
