Wapnir R A, Stiel L
Biochem Med Metab Biol. 1987 Apr;37(2):228-34. doi: 10.1016/0885-4505(87)90031-4.
Metabolic regulation of gluconeogenesis and glycogenolysis by two phosphorylated derivatives of glycerol, G3P, and DHAP, and by F2,6BP, was assessed in vitro in liver homogenates obtained from Chinese hamsters (C. griseus) of two types: diabetic animals from sublines with consistent glycosuria and hyperglycemia, and normoglycemic controls. Only FBPase was sensitive to inhibition by the phosphorylated metabolites. G3P was weakly inhibitory of FBPase. Addition of 7 X 10(-3) M DHAP halved FBPase activity in the diabetic hamsters and 4 X 10(-3) M DHAP produced the same effect in the controls. The other gluconeogenic enzymes and phosphorylase a were only negligibly inhibited. In contrast, F2,6BP inhibited FBPase at concentrations in the micromolar range. Liver homogenates from diabetic hamsters appeared significantly more sensitive to F2,6BP inhibition of FBPase than those from controls at concentrations 0.6 X 10(-6) M and higher. These data indicate that in well-fed hamsters phosphorylated glycerol derivatives are unlikely to regulate hepatic gluconeogenesis at physiologic concentrations. However, the effects of F2,6BP on gluconeogenesis and glycolysis may be linked to those mediated by insulin. Thus, the deficiency of insulin, elevated end-organ insulin resistance, the alteration in the glucagon-insulin interaction, or a combination of these possible causes can be involved in an abnormal regulation of glycolysis and gluconeogenesis at the FBPase step, associated with changes in F2,6BP concentration.
通过甘油的两种磷酸化衍生物甘油-3-磷酸(G3P)和磷酸二羟丙酮(DHAP)以及果糖-2,6-二磷酸(F2,6BP)对糖异生和糖原分解的代谢调节作用,在体外对两种类型的中国仓鼠(黑线仓鼠)肝脏匀浆进行了评估:来自具有持续性糖尿和高血糖的亚系的糖尿病动物,以及血糖正常的对照动物。只有果糖-1,6-二磷酸酶(FBPase)对磷酸化代谢物的抑制敏感。G3P对FBPase有微弱的抑制作用。添加7×10⁻³M的DHAP可使糖尿病仓鼠的FBPase活性减半,而4×10⁻³M的DHAP在对照动物中产生相同效果。其他糖异生酶和磷酸化酶a仅受到微不足道的抑制。相反,F2,6BP在微摩尔范围内的浓度就能抑制FBPase。在浓度为0.6×10⁻⁶M及更高时,糖尿病仓鼠的肝脏匀浆对F2,6BP抑制FBPase的作用似乎比对照仓鼠的肝脏匀浆更为敏感。这些数据表明,在营养良好的仓鼠中,磷酸化甘油衍生物在生理浓度下不太可能调节肝脏糖异生。然而,F2,6BP对糖异生和糖酵解的作用可能与胰岛素介导的作用相关。因此,胰岛素缺乏、终末器官胰岛素抵抗升高、胰高血糖素 - 胰岛素相互作用的改变,或这些可能原因的组合,可能参与了在FBPase步骤中糖酵解和糖异生的异常调节,这与F2,6BP浓度的变化有关。