Carpinelli A R, Malaisse W J
Diabetologia. 1980 Nov;19(5):458-64. doi: 10.1007/BF00281826.
Above a threshold of 3.0-4.2 mmol/l, D-glucose provoked a transient increase in 32P fractional outflow rate from rat pancreatic islets prelabelled with 32P-orthophosphate. Nutrients which stimulate insulin release in the absence of glucose, alpha-ketoisocaproate and L-leucine, also provoked a phosphate flush. No flush occurred in islets exposed to non-insulinotropic nutrients (L-glutamine and and L-lactate) or non-nutriet secretagogues (arginine, tolbutamide, theophylline). A late increase in 32P fractional outflow rate was observed in Ca2+ deprived islets stimulated with BaCl2 and theophylline. The occurrence of a phosphate flush did not appear to be attributable to changes in insulin release, cyclic AMP content, membrane polarisation, K+ conductance, or reduced pyridine nucleotide content. The 32P response to glucose was slightly decreased in the absence of extracellular Ca2+ or HCO3-, markedly impaired in the absence of K4, and virtually abolished in the presence of menadione (10 mumol/l). It is proposed that the occurrence of a phosphate flush is linked to the metabolism of nutrient secretagogues, possibly via an increase in O2 uptake and the production rate of NAD(P)H and ATP.
当D - 葡萄糖浓度高于3.0 - 4.2 mmol/l的阈值时，它会引起预先用32P - 正磷酸盐标记的大鼠胰岛中32P分数流出率短暂增加。在无葡萄糖情况下能刺激胰岛素释放的营养物质，α - 酮异己酸和L - 亮氨酸，也会引起磷酸盐外流。暴露于非促胰岛素营养物质（L - 谷氨酰胺和L - 乳酸）或非营养性促分泌剂（精氨酸、甲苯磺丁脲、茶碱）的胰岛中未出现外流现象。在用BaCl2和茶碱刺激的缺钙胰岛中观察到32P分数流出率后期增加。磷酸盐外流的发生似乎并非归因于胰岛素释放、环磷酸腺苷含量、膜极化、钾离子电导或吡啶核苷酸含量的变化。在无细胞外钙离子或碳酸氢根离子时，对葡萄糖的32P反应略有降低；在无钾离子时，明显受损；而在存在甲萘醌（10 μmol/l）时，几乎完全消失。有人提出，磷酸盐外流的发生与营养性促分泌剂的代谢有关，可能是通过增加氧气摄取以及NAD(P)H和ATP的产生速率实现的。
