Fatty liver is characterised by an accumulation of lipids in hepatic tissue. This can result from alcohol or fructose abuse, leading to alcoholic fatty liver or non-alcoholic fatty liver, respectively. The aetiology of fatty liver is not completely understood, but one line of evidence suggest that a lack dietary choline can increase the risk of its development. This relates to the requirement of choline for the mobilisation of triglycerides to the circulation, without which hepatic lipid accumulation occurs. Phosphatidyl choline (lecithin) is a source of dietary choline present in egg yolks, organ meat, fish and legumes. Structurally lecithin comprises of glycerol, two fatty acids, a phosphate and a choline moiety. Choline can also be synthesised in the body from a methyl group donated to serine. Choline is required because it is needed for the synthesis of the neurotransmitter acetylcholine, but equally importantly choline is a structural component of lecithin. Evidence dating back decades suggests that lecithin may be an essential dietary component.
The importance of choline in clearing fatty acids from the liver has been studied in rats. For example, in one study1 rats were fed a choline deficient diet and injected with radioactive palmitate (palmitate-1-14C). A control group was fed a choline sufficient diet and injected with the same radiolabeled tracer. Those rats fed the choline sufficient diet had a rapid appearance of the radiolabeled palmitate in plasma, suggesting that the fatty acids were not accumulating in hepatic tissues. However, rats fed the choline deficient diets had a slower accumulation of radiolabeled palmitate in their plasma indicative of hepatic lipid accumulation. When the authors analysed the plasma of the rats they found that the lower levels of triglycerides in the plasma of the choline deficient rats was due to the lower specific activity of the very low density lipoprotein (VLDL) particle. Therefore a deficiency of choline in rats impairs the release of triglycerides to circulation, which may be a contributory factor in the development of fatty liver in mammals.
This study stands out from other similar research because the choline deficiency was induced in less than 20 hours. This suggest, in rats at least, that fatty liver can develop quickly in the absence of adequate dietary choline. While rats are not humans, this and other evidence supports the contention that choline is an essential dietary factor in human nutrition. Therefore choline is considered by some to merit promotion to vitamin status, as it is unclear if endogenous synthesis is able to keep pace with metabolic requirements. In addition, the Western diet may exacerbate the rate of development of fatty liver because the high intakes of sugar increase flux through the de novo lipogenesis pathway and increase the formation of hepatic fatty acids. This may increase requirement of choline above endogenous synthesis rates. Consumption of the Western diet in combination with low intakes of choline rich foods may explain the increase in the prevalence of non-alcoholic fatty liver in developed nation in recent years.
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