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The interrelationship of the concentration of hydrogen ions, bicarbonate ions, carbon dioxide and calcium ions in the regulation of renal gluconeogenesis in the rat

机译:氢离子,碳酸氢根离子,二氧化碳和钙离子浓度在大鼠肾糖异生调节中的相互关系

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p1. The interrelationship of acidosis and Casup2+/supon the stimulation of gluconeogenesis by rat kidney-cortex slices was studied. 2. Casup2+/supstimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate, lactate and fructose, but not from galactose. 3. The [Casup2+/sup] needed for optimum gluconeogenesis was about 2mm, but at this concentration, acidosis, produced iin vitro/i by a decrease of [HCOsub3/subsup?/sup] in the medium at constant ip/iCOsub2/sub or by an increase in ip/iCOsub2/sub at constant [HCOsub3/subsup?/sup], did not stimulate gluconeogenesis. 4. In the absence of Casup2+/sup, acidosis (low [HCOsub3/subsup?/sup]) stimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate and lactate but not from fructose or galactose. With succinate as substrate, the stimulatory effect of acidosis (low [HCOsub3/subsup?/sup]) disappeared at Casup2+/supconcentrations above 1.0mm. 5. The [HCOsub3/subsup?/sup] was the most important determinant of the acidosis effect since a decrease of pH caused by an increase in ip/iCOsub2/sub did not uniformly stimulate gluconeogenesis, whereas a decrease in [HCOsub3/subsup?/sup] without a change in pH consistently stimulated glucose formation in a way similar to the stimulation produced by acidosis (low [HCOsub3/subsup?/sup]) in the absence of Casup2+/sup. 6. Acidosis iin vitro/i inhibited the rate of decrease of activity of phosphoenolpyruvate carboxylase in slices, and Casup2+/supcaused an increase in the activity of fructose 1-phosphate aldolase. 7. Respiratory acidosis iin vitro/i caused an increase in the activity of phosphoenolpyruvate carboxylase in kidney cortex and an increase in gluconeogenesis from glutamine. 8. Possible points of interaction between Casup2+/sup, Hsup+/supand HCOsub3/subsup?/supwith the gluconeogenic sequence are discussed./p
机译:> 1。研究了酸中毒和Ca 2 + 与大鼠肾皮质切片刺激糖异生的相互关系。 2. Ca 2 + 刺激谷氨酰胺,谷氨酸,2-氧代戊二酸,琥珀酸,苹果酸,丙酮酸,乳酸和果糖引起的糖异生,但不是半乳糖。 3.最佳糖异生所需的[Ca 2 + ]约为2mm,但在此浓度下,酸中毒通过[HCO 3]的降低在体外产生 ]在恒定 p CO 2 或通过增加 p CO < [HCO 3 ]恒定的sub> 2 不会刺激糖原异生。 4.在缺乏Ca 2 + 的情况下,酸中毒([HCO 3 ]低)刺激了谷氨酰胺,谷氨酸,2-氧戊二酸的糖异生。 ,琥珀酸,苹果酸,丙酮酸和乳酸,但并非来自果糖或半乳糖。以琥珀酸为底物,Ca 2 + 浓度超过1.0mm时,酸中毒(低[HCO 3 ])的刺激作用消失。 5. [HCO 3 ]是酸中毒作用的最重要决定因素,因为 p CO的增加会导致pH降低。 2 不能均匀地刺激糖异生,而[HCO 3 ]的降低却不改变pH值,以相似的方式持续刺激葡萄糖的形成。缺乏Ca 2 + 时酸中毒(低[HCO 3 ])产生的刺激。 6.体外酸中毒抑制了切片中磷酸烯醇丙酮酸羧化酶活性的降低速率,Ca 2+导致果糖1-磷酸醛缩酶活性增加。 7.体外呼吸性酸中毒导致肾皮质中磷酸烯醇丙酮酸羧化酶活性的增加和谷氨酰胺引起的糖异生的增加。 8. Ca 2 + ,H + 和HCO 3 与糖异生序列的可能相互作用点为讨论过。

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