Abstract

Early feed restriction of lambs promotes a permanent mitochondrial dysfunction that impairs feed efficiency along the whole life. Dietary L-carnitine, a compound that plays an essential role in energy metabolism transferring long-chain fatty acids to mitochondria for subsequent β-oxidation, has demonstrated positive effects (e.g., improved markers or muscle/heart function) in early feed restricted lambs. The purpose of the present study is to ascertain the underlying mechanisms under these effects using samples of the same lambs in a liver transcriptomic and metabolomic approach. Twenty-two male Merino lambs were separated from the dams for 9 h daily to allow feed restriction during the suckling period. Once weaned, the lambs were allocated to a control group (CTRL, n = 11) being fed ad libitum a complete pelleted diet during the fattening phase, whereas the second group (CARN, n = 11) received the same diet formulated with 3 g/kg of L-carnitine. The most relevant results of this study revealed that the administration of 3 g of L-carnitine/ kg diet during the fattening period of early feed restricted lambs caused no differential expression of genes involved directly in β-oxidation. However the increased expression of genes related to the excretion of cholesterol as bile acids was in agreement with the higher amounts of glycodeoxycholic acid and other intermediates of cholesterol metabolism in the CARN group, and might have contributed to achieve an improved heart function. Moreover, the increased expression of ribosomes and translation pathways in the liver also allowed explaining the positive effects observed in the CARN group. It can be concluded that the improved markers or muscle/heart function achieved by the administration of 3 g of L-carnitine/kg diet to early feed restricted lambs are caused, mainly, by the increased expression of genes related either to ribosomes or cholesterol excretion.

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