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Summary  1. Two hours after the intraperitoneal injection of 12 mg/kg 1--phenylethylbiguanide (DBI) to guinea pigs fasted 48 h, the 3-hydroxybutyrate/acetoacetate ratio and the concentration of both lactate and pyruvate were increased in the blood of the vena cava. The glucose level and the lactate/pyruvate ratio were not altered. In perfused livers taken from these animals immediately after the blood samples were withdrawn, the rate of glucose formation from lactate was not inhibited. However, the addition of 2×10–5 M DBI to the perfusate caused a 60% suppression of gluconeogenesis under these conditions. — 2. The accumulation of hepatic acetyl-S-Co A with a concomitant decrease of the citrate-and of the 2-oxoglutarate concentration in the presence of DBI indicated an impaired synthesis of citrate. A slight reduction of hepatic oxygen consumption was also consistent with an inhibition of the citric acid cycle. It is concluded that biguanides primarily suppressed hepatic cell respiration, which led to an accumulation of reducing equivalents inside the mitochondria. This may have caused a lack of oxalacetate for mitochondrial citrate synthesis. — 3. The pattern of hepatic metabolite concentrations did not clearly show the rate limiting step of glucose formation from lactate in the presence of biguanides, however, some evidence was found that the conversion of pyruvate to phosphoenolpyruvate was affected. — 4. No exact correlation was found between the effect of DBI on gluconeogenesis and on the hepatic ATP/ADP ratio.

Inhibition of gluconeogenesis from lactate by phenylethylbiguanide in the perfused guinea pig liver