Fatty Liver in Ruminants

The fat content of liver is normally less than 5% of the wet weight. Fatty liver is the condition arising from the progressive infiltration of fat into the liver lobule. Fat content in the liver may increase to 30% of wet weight. Fatty liver is often associated with conditions of undernutrition such as ketosis due to the central role of the liver in the metabolism of fat (Fig. 1). During undernutrition, increased release of NEFA from adipose tissue results in increased uptake of NEFA by liver. In the liver, NEFA can enter the mitochondria for conversion to acetyl CoA and either formation of ketone bodies or complete oxidation. The NEFA that do not enter the mitochondria can be esterified to form phospholipids, cholesterol esters, and triacylglycerols. With adequate glucose availability, CPTI activity is decreased and NEFA are esterified, forming triacylglycerol (TAG).[2] These esterified compounds must be combined with apoproteins and incorporated into very low-density lipoproteins (VLDL) for export from the liver. Hepatic apoB-100 concentration, a component of VLDL, is decreased in cows with ketosis and fatty liver.[5]

In dairy cows, fatty liver is present in early lactation in conjunction with hypoglycemia and negative energy balance. However, evaluation of liver biopsies from cows around calving showed that liver triglyceride content peaked around calving. By day 1 postpartum, approximately half of the cows had more than 15% liver triglyceride. The association of fatty liver with ketosis may be due to impaired gluconeogenic capacity in the liver in conjunction with fatty infiltration.[6] In fatty liver, TAG synthesis in the liver increases and transport of fat in lipoprotein out of the liver decreases. In general, the ability of ruminants to secrete VLDL is lower than that of other species. Decreased secretion may be due to inadequate synthesis of the protein portion of the lipoprotein.

Treatment strategies are designed to decrease lipid mobilization, increase NEFA oxidation, or increase VLDL secretion. Feeding rumen-protected methionine and administration of propylene glycol prepartum or after calving have been used to help decrease hepatic TAG accumulation.1-7-1 Recent research evaluating the effect of a two-week glucagon infusion on TAG content of liver showed a decrease in TAG content from 12.9 to 4.7% following treatment. Glucagon therapy may have practical application if developmental challenges are solved.[8]

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