The interrelationship of acidosis and Ca2+ on the stimulation of gluconeogenesis by rat kidney cortex slices was studied. Ca2+ stimulated gluconeogenesis from glutamine, glutamate, 2 oxoglutarate, succinate, malate, pyruvate, lactate and fructose, but not from galactose. The [Ca2+] needed for optimum gluconeogenesis was about 2 mM, but at this concentration, acidosis, produced in vitro by a decrease of [HCO3-] in the medium at constant pCO2 or by an increase in pCO2 at constant [HCO3-], did not stimulate gluconeogenesis. In the absence of Ca2-, acidosis (low [HCO3-]) 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 [HCO3-]) disappeared at Ca2+ concentrations above 1.0 mM. The [HCO3-] was the most important determinant of the acidosis effect since a decrease of pH caused by an increase in pCO2 did not uniformly stimulate gluconeogenesis, whereas a decrease in [HCO3-] without a change in pH consistently stimulated glucose formation in a way similar to the stimulation produced by acidosis (low [HCO3 -]) in the absence of Ca2+. Acidosis in vitro inhibited the rate of decrease of activity of phosphoenolpyruvate carboxylase in slices, and Ca2+ caused an increase in the activity of fructose 1 phosphate aldolase. Respiratory acidosis in vitro caused an increase in the activity of phosphoenolpyruvate carboxylase in kidney cortex and an increase in gluconeogenesis from glutamine. Possible points of interaction between Ca2+, H+ and HCO3- with the gluconeogenic sequence are discussed.
|Original language||English (US)|
|Number of pages||9|
|State||Published - 1973|
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