Fat accumulation in acute liver injury

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Abstract
In the normal rat there exists a continuous interchange of fat between the fat depots and the liver (a "triglyceride cycle" ). Fat is transported in the form of non-ester if ied fatty acids from the depots to the liver via the blood stream. In the liver it is resynthesized to triglyceride, complexed with protein to form lipoprotein and is secreted into the blood stream almost certainly by the endoplasmic reticulum. It has been suggested that a fatty liver may arise by an interruption of this cycle at the site of exit from the liver. This may be the result of either an inhibition in the synthesis of the protein moiety of lipoprotein or damage to the secretory mechanism. Within 2 h of carbon tetrachloride poisoning, an inhibition to both of these processes takes place, whereas with dimethylnitrosamine, inhibition of protein synthesis precedes damage to the secretory mechanism of the endoplasmic reticulum by many hours. In contrast, thioacetamide, which produces liver necrosis without the accumulation of fat, does not have any effect on the "triglyceride cycle".

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