An inhibitory effect of bicarbonate, administered into rats, on gluconeogenesis within the first 30 min was due to inactivation of the tricarboxylic acid cycle and to deficiency of ATP. Impairment of mitochondrial functions during this period was accompanied by alterations in transport of metabolites, in gluconeogenesis and in turnover of fatty- and amino acids. Insulin prevented mainly these deteriorations but it was also responsible for a specific effect--an increase in gluconeogenesis inhibition during the subsequent period, inhibition of ADP transport from cytosol to mitochondria.

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