Hepatic lipidosis

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Fatty liver in an eight-year-old Friesian cow

Hepatic lipidosis (fatty liver) is a secondary metabolic disease of cattle worldwide, observed more commonly in periparturient dairy cattle.

Similar to other species, hepatic lipidosis has multifactorial causes and is not a 'diagnosis' per se. In cattle, hepatic lipidosis is often associated with negative energy balances around calving[1], where stress, obesity (overconditioned)[2], starvation or sudden weight loss can contribute to sudden demands on metabolic stores of lipids.

Overfeeding energy and higher energy status prepartum has been shown to lead to a surge in insulin and fatty acids. The exposure of hepatocytes to fatty acids elicits inflammation, increase of oxidative stress, apoptosis and production of fibrogenic cytokines[3]. Ketosis is a frequent complications and some cattle may die from subsequent DIC.

Hepatic lipidosis is triggered metabolically by an elevated rise in circulatory nonesterified fatty acid (NEFA), often >1,000 μEq/L. These NEFAs result in formation of ketones (acetoacetate and β-hydroxybutyrate) which lead to a toxic metabolic acidotic state called ketosis.

Clinical signs

Affected cows often present as downer cow syndrome, and have anorexia, reduced milk yield, jaundice and can be triggered or have concurrent mastitis or milk fever. Hepatic lipidosis is common with cows affected by abomasal displacement.

Diagnosis

Presenting clinical signs and ultrasonography[4][5] may lend a suspicion of fatty liver in cattle but confirmation requires laboratory tests, specifically elevations in AST, ALT and Alkaline phosphotase. A liver biopsy is required for definitive diagnosis.

Treatment

Treatment of hepatic lipidosis is aimed at correcting underlying causes, and supportive feeding. Dietary supplementation with choline has shown to minimise fatty esterification within the liver and reduce predisposition in cows to fatty liver syndrome[6].

Glucose is an effective supplement as well as Insulin, which decreases lipid mobilization from adipose tissue.

A single 100 IU IM dose of a 24-hr slow-release insulin immediately after calving may be prophylactic[7].

References

  1. Li P et al (2012) Alterations of fatty acid β-oxidation capability in the liver of ketotic cows. J Dairy Sci 95(4):1759-1766
  2. Graugnard DE et al (2012) Blood immunometabolic indices and polymorphonuclear neutrophil function in peripartum dairy cows are altered by level of dietary energy prepartum. J Dairy Sci 95(4):1749-1758
  3. Chavez-Tapia NC et al (2012) Effect of intracellular lipid accumulation in a new model of non-alcoholic fatty liver disease. BMC Gastroenterol 12:20
  4. Tharwat M et al (2012) Ultrasonography as a diagnostic and prognostic approach in cattle and buffaloes with fatty infiltration of the liver. Pol J Vet Sci 15(1):83-93
  5. Weijers G et al (2012) Transcutaneous vs. Intraoperative Quantitative Ultrasound for Staging Bovine Hepatic Steatosis. Ultrasound Med Biol 38(8):1404-1413
  6. Zom RL et al (2011) Effect of rumen-protected choline on performance, blood metabolites, and hepatic triacylglycerols of periparturient dairy cattle. J Dairy Sci 94(8):4016-4027
  7. Merck Vet Manual