Summary
The purpose of these studies was to determine if the utilization of ketone bodies
as a carbon source for lipogenesis could account for the decreased ketone body production
by livers of obese Zucker rats, as well as contribute to the enhanced rates of fatty
acid synthesis observed in these animals. Ketone body production was decreased from
822 μmol/liver in the lean to 538 μmol/liver in the obese genotype (P < 0.05). The
incorporation of ketone bodies into fatty acids was significantly greater in the obese
rat liver (lean, 1.95 μmol of ketone bodies/liver, versus obese, 35.22 μmol/liver;
P < 0.025). The relative contribution of this pathway to the overall rate of fatty
acid synthesis was not affected by genotype and accounted for only 3 to 4% of the
fatty acids synthesized. The incorporation of ketone bodies into digitonin precipitable
sterols was similar in the two genotypes (lean, 4.5 mmol/liver, versus obese 4.7 μmol/liver;
NS). This accounted for 9.2 and 6.3% of the total sterol synthesis in lean and obese
rat livers, respectively. The total incorporation of ketone bodies into lipid was
7.5 μmols in the lean rat livers and 42.0 μmoles in the obese (P < 0.025). The net
increase was 35 μmoles incorporated, whereas the net decrease in ketogenesis was 284
μmoles. Thus, although ketone body carbon utilization for lipid synthesis was increased
in the liver of the obese rats, this pathway could only account for a fraction of
the genotypic difference in ketone body production and was of relatively minor importance
as a source of carbon for hepatic fatty acid synthesis in both lean and obese rats.
Key words
Ketone Bodies - Fatty Acid Synthesis - Genetic Obesity
