TY - JOUR
T1 - The effect of acetaldehyde on gluconeogenesis from xylitol, sorbitol, and fructose by isolated rat liver cells
AU - Cederbaum, Arthur I.
AU - Dicker, Elisa
N1 - Funding Information:
‘These studies were supported by Research Scientist Career Development Award 5 K02-AA-0003 from the National Institute on Alcohol Abuse and Alcoholism, Mount Sinai Alcohol Research Center Grant AA-03508, and NIH Grant AA-03312.
PY - 1979/10/15
Y1 - 1979/10/15
N2 - In isolated rat liver cells, ethanol inhibited gluconeogenesis from xylitol and sorbitol but not from fructose. Acetaldehyde, at initial concentrations of 0.2, 0.5, and 1.0 mm, stimulated gluconeogenesis from xylitol and sorbitol in the absence of pyrazole but inhibited in the presence of pyrazole. There was no effect with fructose. Acetate had no effect. Methylene blue and pyruvate (but not lactate) prevented the stimulatory as well as the inhibitory effects of acetaldehyde. Acetoacetate (but not β3-hydroxybutyrate) prevented, to a large extent, the inhibitory effects of low (but not high) concentrations of acetaldehyde. The inhibition by low concentrations of acetaldehyde appears to be mediated via acetaldehyde oxidation in the mitochondria, whereas the inhibition by high concentrations of acetaldehyde appears to reflect acetaldehyde oxidation in the cytosol. These data indicate that the inhibitory action of ethanol on glucose production from xylitol and sorbitol can be reproduced by physiological concentrations of acetaldehyde. Changes in the NAD+ NADH ratio produced during acetaldehyde metabolism appear to be responsible for these effects of acetaldehyde. These changes may contribute to the actions of ethanol on gluconeogenesis from these substrates.
AB - In isolated rat liver cells, ethanol inhibited gluconeogenesis from xylitol and sorbitol but not from fructose. Acetaldehyde, at initial concentrations of 0.2, 0.5, and 1.0 mm, stimulated gluconeogenesis from xylitol and sorbitol in the absence of pyrazole but inhibited in the presence of pyrazole. There was no effect with fructose. Acetate had no effect. Methylene blue and pyruvate (but not lactate) prevented the stimulatory as well as the inhibitory effects of acetaldehyde. Acetoacetate (but not β3-hydroxybutyrate) prevented, to a large extent, the inhibitory effects of low (but not high) concentrations of acetaldehyde. The inhibition by low concentrations of acetaldehyde appears to be mediated via acetaldehyde oxidation in the mitochondria, whereas the inhibition by high concentrations of acetaldehyde appears to reflect acetaldehyde oxidation in the cytosol. These data indicate that the inhibitory action of ethanol on glucose production from xylitol and sorbitol can be reproduced by physiological concentrations of acetaldehyde. Changes in the NAD+ NADH ratio produced during acetaldehyde metabolism appear to be responsible for these effects of acetaldehyde. These changes may contribute to the actions of ethanol on gluconeogenesis from these substrates.
UR - http://www.scopus.com/inward/record.url?scp=0018616648&partnerID=8YFLogxK
U2 - 10.1016/0003-9861(79)90263-7
DO - 10.1016/0003-9861(79)90263-7
M3 - Article
C2 - 228600
AN - SCOPUS:0018616648
SN - 0003-9861
VL - 197
SP - 415
EP - 423
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
IS - 2
ER -