Disturbed bovine mitochondrial lipid metabolism: a review

In mammals, excess energy is stored primarily as triglycerides, which are mobilized when energy demands arise and cannot be covered by feed intake. This review mainly focuses on the role of long chain fatty acids in disturbed energy metabolism of the bovine species. Long chain fatty acids regulate energy metabolism as ligands of peroxisome proliferator-activated receptors. Carnitine acts as a carrier of fatty acyl groups as long-chain acyl-CoA derivatives do not penetrate the mitochondrial inner membrane. There are two different types of disorders in lipid metabolism which can occur in cattle, namely the hypoglycaemic-hypoinsulinaemic and the hyperglycaemic-hyperinsulinaemic type with the latter not always associated with ketosis. There is general agreement that fatty acid β-oxidation capability is limited in the liver of (ketotic) cows. In accord, supplemental L-carnitine decreased liver lipid accumulation in periparturient Holstein cows. Of note, around parturition concurrent oxidation of fatty acids in skeletal muscle is highly activated. Also peroxisomal β-oxidation in liver of dairy cows may be part of the hepatic adaptations to a negative energy balance (NEB) to break down fatty acids. An elevated blood concentration of nonesterified fatty acids is one of the indicators of NEB in cattle among others like increased β-hydroxy butyrate concentration, and decreased concentrations of glucose, insulin, and insulin-like growth factor-I. Assuming that liver carnitine concentrations might limit hepatic fatty acid oxidation capacity in dairy cows, further study of the role of acyl-CoA dehydrogenases and/or riboflavin in bovine ketosis is warranted.