García-Salguero L, Lupiáñez J A
Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias, Universidad de Granada, Spain.
Mol Cell Biochem. 1988 Oct;83(2):167-78. doi: 10.1007/BF00226144.
The influence of starvation on renal carbohydrate metabolism was studied in the proximal and distal fragments of the nephron. Starvation induced a double and opposite adaptation mechanism in both fractions of the renal tubule. In renal proximal tubules, the gluconeogenic flux was stimulated progressively during a period of 48 hours of starvation (2.15 fold), due, in part, to a significant increase in the fructose 1,6-bisphosphatase and phosphoenolpyruvate carboxykinase activities although with different characteristics. Fructose 1,6-bisphosphatase activity from this tubular fragment increased only at subsaturating subtrate concentration (68%) which involved a significant decrease in the Km (35%) for fructose 1,6-bisphosphate while there was no change in Vmax. This behaviour clearly indicates that it is related to modifications in the activity of the preexistent enzyme in the cell. Proximal phosphoenolpyruvate carboxykinase activity increased proportionally at both substrate concentrations (86 and 89% respectively) which brought about changes in Vmax without changes in Km, all of which are in accordance with variations in the cellular levels of the enzyme. In the renal distal tubules, the glycolytic capacity drastically decreased throughout the starvation time. At 48 hours 65% of inhibition was shown. We have found a short term regulation of phosphofructokinase activity by starvation which involves an increase in Km (2.2 fold) without changes in Vmax, as a result of these kinetic changes, an inactivation of phosphofructokinase was detected at subsaturating concentration of fructose 6-phosphate. On the contrary, this nutritional state did not modify the kinetic behaviour of renal pyruvate kinase. Finally, neither proximal glycolytic nor distal gluconeogenic capacities and related enzymes activities were changed during starvation.
研究了饥饿对肾单位近端和远端片段肾碳水化合物代谢的影响。饥饿在肾小管的两个部分诱导了双重且相反的适应机制。在肾近端小管中，饥饿48小时期间糖异生通量逐渐受到刺激（增加2.15倍），部分原因是果糖1,6 - 二磷酸酶和磷酸烯醇式丙酮酸羧激酶活性显著增加，尽管具有不同特征。来自该肾小管片段的果糖1,6 - 二磷酸酶活性仅在亚饱和底物浓度下增加（68%），这涉及果糖1,6 - 二磷酸的Km显著降低（35%），而Vmax没有变化。这种行为清楚地表明它与细胞中预先存在的酶活性的改变有关。近端磷酸烯醇式丙酮酸羧激酶活性在两种底物浓度下均成比例增加（分别为86%和89%），这导致Vmax发生变化而Km不变，所有这些都与该酶的细胞水平变化一致。在肾远端小管中，整个饥饿期间糖酵解能力急剧下降。在48小时时显示出65%的抑制率。我们发现饥饿对磷酸果糖激酶活性有短期调节作用，这涉及Km增加（2.2倍）而Vmax不变，由于这些动力学变化，在果糖6 - 磷酸亚饱和浓度下检测到磷酸果糖激酶失活。相反，这种营养状态并未改变肾丙酮酸激酶的动力学行为。最后，饥饿期间近端糖酵解能力和远端糖异生能力以及相关酶活性均未改变。
