Achs M J, Garfinkel L, Garfinkel D
Department of Computer Science, University of Pennsylvania, Moore School of Electrical Engineering, Philadelphia 19104.
J Theor Biol. 1991 May 7;150(1):109-35. doi: 10.1016/s0022-5193(05)80478-3.
We have modeled an experiment with perifused pancreatic islet cells using our BIOSSIM language. The experiment and the resulting model are concerned with glucose uptake and glycolysis by the beta-cells of pancreatic islets. Although glycolysis appears to be involved in insulin release, we do not have enough information to represent insulin release in detail. The rapid entry of glucose into the beta-cell is promoted by a carrier having a very high tissue capacity. Phosphorylation of glucose by the low affinity enzyme glucokinase appears to be limiting for glycolysis. The effects of several hexose diphosphate activators of phosphofructokinase are modeled. Model behavior is described. The kinetic parameters of the enzyme submodels are given. Because of the difficulties of preparing large amounts of experimental material, information on pancreatic islet metabolism is limited. This model is a plausible explanation of the experimental results. Recent work on the genetically engineered glucose transporter and glucokinase is discussed.
我们使用BIOSSIM语言对灌注的胰岛细胞实验进行了建模。该实验及所得模型涉及胰岛β细胞的葡萄糖摄取和糖酵解。尽管糖酵解似乎与胰岛素释放有关，但我们没有足够的信息来详细描述胰岛素释放。具有非常高组织容量的载体促进葡萄糖快速进入β细胞。低亲和力酶葡萄糖激酶对葡萄糖的磷酸化似乎是糖酵解的限制因素。对磷酸果糖激酶的几种己糖二磷酸激活剂的作用进行了建模。描述了模型行为。给出了酶子模型的动力学参数。由于制备大量实验材料存在困难，关于胰岛代谢的信息有限。该模型是对实验结果的一种合理的解释。讨论了关于基因工程葡萄糖转运体和葡萄糖激酶的最新研究。
