Coconut oil is commonly used to enhance the energy content of infant formulas due to its high medium-chain fatty acid (MCFA) content. Using neonatal pigs as model for the human infant, we previously reported that feeding a formula rich in MCFA led to hepatic fat accumulation compared to an isocaloric long-chain fatty acid formula (LCFA). In addition, isolated hepatocytes from MCFA fed pigs oxidized more glutamate than LCFA fed pigs, suggesting a shift in liver metabolism. Thus, the objectives of this study were to investigate whether MCFA and LCFA feeding affect hepatic laurate (C12:0), and palmitate (C16:0) oxidation, and determine whether fat type influences the expression of genes related to fatty acid metabolism in the liver. Twenty-six, 3-day-old pigs were allotted one of three sow milk replacer formulas: a control (CONT) formula that provided 80% of caloric requirements, and two isocaloric formulas that provided 120% of caloric requirements with fat either as LCFA or MCFA. Pigs were fed 250 ml∙kg-1∙day-1 for 22 days, weights were determined every other day, and formula allowance adjusted accordingly. Body composition was determined using DXA at day -1 and 21. On day 22, pigs were euthanized. Muscle and organs were excised, weighed, and sampled. Liver samples were homogenized and incubated with [2-C14]palmitate or [2-C14]laurate. Following a 60 min incubation, radio-labelled enrichment of CO2 and acid-soluble metabolites were determined. Fat was extracted from liver samples using a modified Bligh and Dyer method, fatty acids were methylated to fatty acid methyl esters, and their concentrations determined by gas chromatography/mass spectrometry. Expression of genes related to fatty acid metabolism was determined using Real-Time PCR. In addition, citrate synthase (CS) activity was measured in liver homogenates using spectrophotometry. Body weight of pigs fed the LCFA formula was greater (8.3%) than those fed the MCFA and CONT formulas (P lt; 0.05). In addition, LCFA lean tissue mass was greater (29%) when compared with CONT while MCFA was intermediate (P lt; 0.05). Liver weight of MCFA pigs was 25 and 77% greater than LCFA and CONT groups (P lt; 0.05). Liver fat was greater (142%) for MCFA pigs compared with LCFA and CONT counterparts (P lt; 0.05). Palmitate and laurate oxidation to CO2 was greater (49%) for pigs fed the LCFA and CONT formulas compared with those fed MCFA (P lt; 0.05). In addition, complete oxidation of palmitate and laurate was greater (112%) for LCFA and CONT pigs (P lt; 0.05). MCFA fed pigs had greater proportions of laurate, myristate and palmitate in their livers compared with LCFA and CONT groups (P lt; 0.05). Expression of fatty acid synthase 3 (FASN-3), fatty acid binding protein 1(FABP-1), and acetyl CoA carboxylase 1 (ACACA-1) were 8, 6, and 2-fold greater for the MCFA pigs than LCFA and CONT pigs (P lt; 0.05). However, apolipoprotein-B (APO-B) expression was not affected by treatment. These data suggest that feeding a formula rich in MCFA led to hepatic steatosis, and that fatty acid composition in liver did not reflect that of fed formulas. In addition, liver steatosis in pigs fed the MCFA rich formula is correlated with a reduction in the liver’s ability to oxidize fatty acids when compared with pigs fed an isocaloric LCFA based formula.
