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Dietary phospholipid alters biliary lipid composition in formula-fed piglets
1Department of Paediatrics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Lipids
|February 1, 2000
Summary
Supplementing infant formula with arachidonic acid (AA) and docosahexaenoic acid (DHA) from egg phospholipids improves bile lipid metabolism. This enhances bile AA and DHA concentrations, alongside bile acid and phospholipid levels.
Area of Science:
- Nutritional Biochemistry
- Lipid Metabolism
- Infant Nutrition
Background:
- Breast-fed infants exhibit higher plasma levels of cholesterol, arachidonic acid (AA), and docosahexaenoic acid (DHA) compared to formula-fed infants.
- Egg phospholipids are a source of AA and DHA, crucial fatty acids for infant development.
Purpose of the Study:
- To investigate the impact of supplementing infant formula with cholesterol and egg phospholipid-derived AA and DHA on plasma, hepatic, and bile lipids.
- To assess changes in hepatic protein expression related to sterol metabolism.
Main Methods:
- Three groups of piglets were fed: formula with cholesterol, formula with cholesterol and egg phospholipid (providing AA and DHA), and sow milk.
- Plasma, hepatic, and bile lipid profiles, phospholipid fatty acid composition, and gene expression of key metabolic enzymes were analyzed.
Main Results:
- Formula supplemented with egg phospholipid AA and DHA increased plasma high-density lipoprotein cholesterol and bile acid and phospholipid concentrations.
- Liver and bile phospholipid levels of AA and DHA were significantly higher in piglets fed supplemented formula.
- While hepatic enzyme mRNA levels (HMG-CoA reductase, 7-alpha-hydroxylase) were not different between supplemented and unsupplemented formula groups, they were higher than in the sow milk group.
Conclusions:
- Supplementing infant formula with AA and DHA from egg phospholipids positively alters bile metabolism.
- This supplementation increases the concentration of AA, DHA, bile acids, and phospholipids in bile, supporting infant lipid homeostasis.