Intestinal absorption, blood transport and hepatic and muscle metabolism of fatty acids in preruminant and ruminant animals

Current research on Lipid metabolism in ruminants aims to improve the growt h and health of the animals and the muscle characteristics associated with meat quality. This review, therefore, focuses on fatty acid (FA) metabolism from absorption to partitioning between tissues and metabolic pathways. In young calves, which were given high-fat milk diets, lipid absorption is de layed because the coagulation of milk caseins results in the retention of d ietary fat as an insoluble clot in the abomasum. After weaning, the calves were fed forage- and cereal-based diets containing low levels of long-chain fatty acids (LCFA) but leading to high levels of volatile fatty acid (VFA) production by the rumen microflora. Such differences in dietary FA affect: i) the lipid transport system via the production of lipoproteins by the in testine and the liver; and (ii) the subsequent metabolism of lipids and FA by tissues. In preruminant calves, high-fat feed stimulates the secretion o f triacylglycerols (TG)-rich lipoproteins (chylomicrons, very-low density l ipoproteins (VLDL)). Diets rich in polyunsaturated FA (PUFA) stimulate the production of chylomicrons by the intestine (at peak lipid absorption) and of high density lipoproteins by the liver, leading to high blood concentrat ions of cholesterol. High levels of non-esterified FA (NEFA) uptake by the liver in high-yielding dairy cows in early lactation leads to TG infiltrati on of the hepatocytes (fatty liver). This is due to the low chronic capacit y of the liver to synthesise and secrete VLDL particles. This abnormality i n hepatic FA metabolism involves defects in apolipoprotein B synthesis and low availability of apolipoproteins and lipids for VLDL packaging. Fatty li ver in calves is also caused by milk diets containing either soybean oil (r ich in n-6 PUFA), or coconut oil (rich in C12:0 and C14:0). The ability of muscle tissue to use FA as an energy source depends on its mitochondrial co ntent and, hence, on many physiological factors. The uptake and partitionin g of LCFA between oxidation and storage in muscle is regulated by the activ ity of key intracellular enzymes and binding proteins. One such protein, ca rnitine palmitoyltransferase I (CPT I) controls the transport of LCFA into mitochondria. Metabolites derived from LCFA inhibit glucose oxidation, decr ease the activity of CPT I and decrease the efficiency of ATP production by mitochondria. Most research on tissue lipid metabolism in ruminants is foc used on: i) the partitioning of FA oxidation between intracellular peroxiso mes and mitochondria in the liver and in muscles; (ii) the regulation of li pid metabolism by leptin, a recently discovered hormone secreted by mature adipocytes; and iii) the effects of activation of the nuclear receptors (PP ARs and RXR) by LCFA or by phytol metabolites derived from chlorophyll. (C) Inra/Elsevier, Paris.