Rognstad R
Biochem Biophys Res Commun. 1984 Jul 31;122(2):726-33. doi: 10.1016/s0006-291x(84)80094-7.
In hepatocytes from fasted rats, Zn2+ in the range from 0 to 500 microM has relatively minor effects on gluconeogenesis from most substrates, or on ureagenesis from NH3. In hepatocytes from fed rats, Zn2+ does not affect glycogenolysis. In hepatocytes from fasted rats, in which glycogen is being actively synthesized using the substrate combination (Katz et al. (1976) Proc. Natl.Acad.Sci.USA 73,3433-3437) of glucose, lactate and glutamine (all 10mM), Zn2+ markedly inhibits glycogen synthesis, with total inhibition at 500 microM, and a half maximal effect in the range from 50 to 100 microM. Dipicolinate (pyridine 2,6-dicarboxylate), a zinc chelator, is about as effective as L-glutamine in activating glycogen synthesis with the substrate combination of dihydroxyacetone, lactate and glucose (all 10mM). This suggests the possible hypothesis that endogenous Zn2+ might control the rate of glycogen synthesis in vivo. However, alternate explanations such as metabolite accumulation are also possible, since dipicolinate causes inhibition of gluconeogenesis from L-lactate.
在禁食大鼠的肝细胞中，浓度范围为0至500微摩尔的锌离子对大多数底物的糖异生或氨的尿素生成影响相对较小。在喂食大鼠的肝细胞中，锌离子不影响糖原分解。在禁食大鼠的肝细胞中，此时正使用葡萄糖、乳酸和谷氨酰胺（均为10毫摩尔）的底物组合（卡茨等人，《美国国家科学院院刊》，1976年，第73卷，第3433 - 3437页）积极合成糖原，锌离子显著抑制糖原合成，在500微摩尔时完全抑制，在50至100微摩尔范围内有半数最大效应。二吡啶甲酸盐（吡啶 - 2,6 - 二羧酸盐），一种锌螯合剂，在用二羟基丙酮、乳酸和葡萄糖（均为10毫摩尔）的底物组合激活糖原合成方面与L - 谷氨酰胺效果相当。这提示了一种可能的假说，即内源性锌离子可能在体内控制糖原合成速率。然而，诸如代谢物积累等其他解释也是有可能的，因为二吡啶甲酸盐会抑制L - 乳酸的糖异生。
