In our earlier paper (Kalapos et al., Int. J. Biochem. 26, 1069-1079, 1994) we described that the contribution of acetone to net glucose formation in isolated murine hepatocytes was only possible when alanine was present. The aim of the present work was to investigate whether the above mentioned phenomenon was specific to alanine. Hepatocytes were prepared from 48 hr-starved mice maintained on untreated or acetone-treated drinking water. Glucose production was determined in cells after 30 min incubation with different gluconeogenic substrates using glucose oxidase/peroxidase method. Glucose formation from glycerol, fructose, alanine, methylglyoxal, and lactate was increased by the addition of acetone in hepatocytes prepared from 48 hr-starved animals, while acetone reduced glucose production in the cells which originated from acetone pretreated 48 hr-starved mice. However, a higher rate of glucose production from 1 mM pyruvate in combination with 1 mM acetone compared with glucose production from 1 mM pyruvate was observed, in hepatocytes originated from starved animals without and with acetone pretreatment glucose formation, expressed in nmol glucose/106 cells, was elevated from 172.3 ± 21.4 (SEM, n = 5) to 205.3 ± 29.0 (SEM, n = 5, P < 0.05) and from 164.9 ± 20.2 (SEM, n = 5) to 195.2 ± 14.0 (SEM, n = 5, P < 0.05), respectively. In summary, the action of acetone on glucose production from gluconeogenic substrates is not restricted to alanine, as a substrate. It is concluded that acetone may play a role in maintenance of hepatic glucose output in ketonemia and may do so by using a wide range of substrates for NADPH + H+ generation which, as a cofactor, is needed for the cytochrome P450s to metabolize acetone.
|Number of pages||5|
|Journal||International Journal of Biochemistry and Cell Biology|
|Publication status||Published - Jun 1996|
ASJC Scopus subject areas
- Cell Biology