Regulation of Fatty Acid Synthesis in the Liver of Prenatal and Early Postnatal Chicks
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TL;DR
O-glycerophosphate is not a direct regulator of the total activities of acetyl-CoA carboxylase or fatty acid synthetase in embryonic chicks, and it is not appropriate for intermediates which may regulate both the rate of fatty acid synthesis and the concentration of the lipogenic enzymes.
Abstract
Abstract A normal mash diet or a single glucose injection stimulates fatty acid synthesis and increases the total activities of acetyl coenzyme A carboxylase, fatty acid synthetase, and malic enzyme in the livers of neonatal chicks. Feeding and glucose injection caused a decrease in the concentration of free fatty acids and fatty acyl-CoA and an increase in α-glycerophosphate and free CoA. These concentration changes are appropriate for intermediates which may regulate both the rate of fatty acid synthesis and the concentration of the lipogenic enzymes. The hepatic concentrations of citrate and acetyl-CoA were unaffected by feeding or glucose injection. During the hatching process, total activities of acetyl-CoA carboxylase and fatty acid synthetase in the liver increased but the rate of fatty acid synthesis did not. Concomitantly, free stearate in the liver decreased, but none of the other metabolites indicated above were affected. Fatty acid synthetase increased and hepatic free stearate decreased when embryos were incubated in 100% oxygen. Stearate or a metabolite derived from stearate is a potential negative regulator of the concentration of fatty acid synthetase in chick liver. Injection of glucose into 18-day-old embryos markedly increased the α-glycerophosphate content of the liver but had no effect on the total activities of the lipogenic enzymes. Hence, α-glycerophosphate is not a direct regulator of the total activities of acetyl-CoA carboxylase or fatty acid synthetase in embryonic chicks.
