Cholesterol and fatty acid metabolism in piglets fed sow milk or infant formula with or without addition of cholesterol

Abstract

Several studies have reported that plasma cholesterol and phospholipid (PL) levels of arachidonic acid (20:4n−6) are lower and PL levels of linoleic acid (18:2n−6) are higher in infants fed formula than in infants fed human milk. Plasma cholesterol level 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 used for esterification of plasma free cholesterol. Whether the low cholesterol content of infant formula as compared with human milk is related to the difference in plasma n−6 fatty acid levels between infants fed human milk and infants fed formula is not known. This study determined the effect of feeding formula with 0.05 mmol cholesterol/L, formula with 1.09 mmol cholesterol/L, or sow milk with 0.34 mmol cholesterol/L on plasma, liver, and bile lipid fatty acid levels and liver low-density lipoprotein (LDL) receptor mass in piglets. Liver microsomal 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity and plasma lathosterol were assayed as indices of liver and body cholesterol synthesis, respectively. Formula with or without cholesterol added, or sow milk, was fed from birth to 18 days of age. Providing cholesterol in the formula did not correct the significantly lower plasma cholesterol or plasma and liver PL 20:4n−6 levels associated with formula feeding. The liver total cholesterol and cholesteryl esters (CE), biliary bile acid, and PL concentrations 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 added. No evidence of fewer hepatic LDL receptors was found in piglets fed sow milk compared with piglets fed formula. The results show marked differences in hepatic and bile n−6 fatty acid concentrations between artificially and naturally fed piglets that were not explained by the difference in dietary cholesterol intake alone. The significance of the changes in bile lipid composition due to formula feeding should be studied further.