The role of oleic acid and cholesterol in neonatal diet

Oleic acid (18:1) and cholesterol are not considered to be essential dietary nutrients for adults or infants. Human milk provides a significant amount of each of these nutrients. In contrast, most infant formulas contain relatively low 18:1 and cholesterol. The overall objective of this thesis was to determine the importance of 18:1 and cholesterol in natural milk to infant nutrition. Recent studies found reduced 18:1 in brain total lipid of piglets fed formula with 17% 18:1 rather than sow milk providing 37% 18:1. Oleic acid is a major fatty acid in brain myelin lipid and is rapidly deposited during myelination. It is important, therefore, to know if reduced 18:1 in brain total lipid reflects deposition of myelin lipid with reduced 18:1 and/or delayed myelination, or is related to changes in other brain membranes. The first part of this thesis determined the fatty acid composition of myelin total lipid, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) and of plasma and liver phospholipid (PL) from piglets fed from birth to 15 d with formula containing low (17%) or high (38%) 18:1, or sow milk. Brain 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP'ase) activity and cerebrosides concentration were also determined and used as indicators of myelination. Piglets fed the low 18:1 formula had lower 18:1 in their plasma and liver PL than sow milk-fed piglets. Formula providing a similar level of 18:1 to sow milk resulted in higher 18:1 in piglet plasma and liver PL than in sow milk-fed piglets. Brain cerebrosides and CNP'ase activity and myelin 18:1 were similar in sow milk- and formula-fed piglets, irrespective of the formula 18:1 content. These studies suggest that supplying 18:1 in formula in a similar quantity to natural milk is not essential to normal accretion of 18:1 in brain myelin. Several studies have reported that plasma cholesterol and PL levels of 20:4n-6 are lower and PL levels of 18:2n-6 are higher in infants fed formula than in infants fed human milk. Plasma cholesterol and possibly the dietary intake of cholesterol, could be related to plasma PL n-6 fatty acid metabolism because plasma PL 18:2n-6 is usually used for esterification of plasma free cholesterol. Whether the low cholesterol content of infant formula compared to human milk is related to the difference in plasma n-6 fatty acids between infants fed human milk and formula is not known. The second part of this thesis determined the effect of feeding a formula containing low (0.05 mmol/L) or high (1.09 mmol/L) cholesterol content, or sow milk, on plasma, liver and bile lipid fatty acids and liver LDL receptor mass in piglets fed from birth to 18 days. Liver microsomal HMG CA reductase activity and plasma lathosterol were assayed as indices of liver and body cholesterol synthesis, respectively. Providing cholesterol in the formula did not correct the significantly lower plasma cholesterol, or plasma and liver PL 20:4n-6 associated with formula feeding. The liver total cholesterol and cholesterol esters, biliary bile acids and PL concentration were significantly higher and the liver HMG CoA reductase activity and plasma lathosterol:cholesterol ratio were significantly lower in piglets fed the formula with cholesterol than in piglets fed the formula without cholesterol. No evidence of lower hepatic LDL receptor mass was found in piglets fed sow milk compared to piglets fed formula. The results show marked differences in hepatic and bile n-6 fatty acid concentration between artificially and naturally fed piglets which do not seem to be explained by the difference in dietary cholesterol intake. Whether or not cholesterol and 18:1 should be added to infant formula in concentrations similar to that of natural milk is still unknown. Results from this thesis do not provide evidence that they should be added.Land and Food Systems, Faculty ofGraduat