Bedoya F J, Oberholtzer J C, Matschinsky F M
J Histochem Cytochem. 1987 Oct;35(10):1089-93. doi: 10.1177/35.10.3305701.
Glucose phosphorylation was studied in B-cell-enriched or in B-cell-depleted pancreatic islets from normal or streptozotocin-diabetic rats, respectively, using quantitative histochemical procedures. The data indicate that B-cell-enriched preparations from normal animals and whole islets from normals, diabetics, and insulin-treated diabetic animals have comparable glucokinase activities. Average maximum velocities were (mmol/kg dry tissue/hr) 134.1 +/- 7.3 for whole islets and 125.6 +/- 10.7 for the B-cell-enriched preparations from normal rats, 143.1 +/- 13.6 for B-cell-depleted islets from diabetic rats, and 124.4 +/- 10.7 for B-cell-depleted islets from insulin-treated diabetic animals. The Kmax for glucose of the enzyme in islets from untreated diabetic rats was 16 mM, comparable to the Kmax found for glucokinase from normal rat islets. Mannoheptulose, previously shown to be a competitive inhibitor of glucokinase from liver and normal islets, also inhibited glucokinase in B-cell-depleted islets from diabetic rats. The data indicate that glucokinase is not selectively located in the B-cell, as was previously assumed, but is also found in A- and/or D-cells of diabetic rats. This observation raises significant questions about the functional role of islet glucokinase under control and diabetic conditions.
采用定量组织化学方法，分别对正常大鼠或链脲佐菌素诱导的糖尿病大鼠的富含B细胞或去除B细胞的胰岛中的葡萄糖磷酸化进行了研究。数据表明，正常动物的富含B细胞的制剂以及正常、糖尿病和胰岛素治疗的糖尿病动物的整个胰岛具有相当的葡萄糖激酶活性。平均最大速度为（mmol/kg干组织/小时）：正常大鼠的整个胰岛为134.1±7.3，富含B细胞的制剂为125.6±10.7；糖尿病大鼠去除B细胞的胰岛为143.1±13.6；胰岛素治疗的糖尿病动物去除B细胞的胰岛为124.4±10.7。未治疗的糖尿病大鼠胰岛中该酶对葡萄糖的Kmax为16 mM，与正常大鼠胰岛中葡萄糖激酶的Kmax相当。甘露庚酮糖先前已被证明是肝脏和正常胰岛中葡萄糖激酶的竞争性抑制剂，它也能抑制糖尿病大鼠去除B细胞的胰岛中的葡萄糖激酶。数据表明，葡萄糖激酶并非如先前假设的那样选择性地位于B细胞中，在糖尿病大鼠的A细胞和/或D细胞中也能发现。这一观察结果对正常和糖尿病状态下胰岛葡萄糖激酶的功能作用提出了重大问题。
