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Lecithin:cholesterol acyltransferase (LCAT) activity during lipid infusion in premature infants
Insights
Premature infants have low lecithin: cholesterol acyltransferase (LCAT) activity. Intralipid infusions did not impair cholesterol metabolism in preterm infants at recommended doses, suggesting prematurity, not Intralipid, may cause low LCAT activity.
Area of Science:
- Biochemistry
- Neonatal Medicine
- Lipid Metabolism
Background:
- Lecithin: cholesterol acyltransferase (LCAT) regulates plasma cholesterol.
- Premature infants exhibit low cord blood LCAT activity.
- Hypercholesterolemia in infants receiving Intralipid may stem from low LCAT activity.
Purpose of the Study:
- Quantify serum LCAT activity in preterm infants on total parenteral nutrition (TPN).
- Investigate the impact of Intralipid infusions on LCAT activity and lipid profiles in preterm neonates.
- Determine if Intralipid administration affects LCAT activity or cholesterol metabolism in premature infants.
Main Methods:
- LCAT activity, apoprotein A1, cholesterol, triglycerides, and free fatty acids were measured in eleven premature infants on TPN.
- Infants received daily Intralipid infusions at 0.5-2.0 g/kg/day for 15 hours.
- Blood samples were collected pre-infusion and before completion.
Main Results:
- LCAT activity and apoprotein A1 levels were significantly lower than adult levels (21-24% and 30-35%, respectively).
- Despite low LCAT activity, serum cholesterol levels remained within the normal range during Intralipid infusion.
- Intralipid administration at 0.5-2.0 g/kg/day did not appear to impair Intralipid-lecithin clearance or cholesterol metabolism.
Conclusions:
- Low LCAT activity and apoprotein A1 levels in preterm infants may be linked to prematurity or lack of enteral feeding rather than Intralipid.
- Intralipid infusion at rates up to 1-2 g/kg/day seems safe regarding cholesterol metabolism in preterm infants.
- Further research is needed to elucidate the exact causes of low LCAT activity in this population.
Abstract:
Plasma cholesterol and lecithin concentrations are regulated by the serum enzyme lecithin: cholesterol acyltransferase (LCAT). LCAT activity is low in cord blood of premature infants, suggesting that in these infants the hypercholesterolemia associated with Intralipid infusion might be due to low LCAT activity. The serum LCAT activity has not been quantitated in preterm infants receiving intravenous fat emulsions. We have therefore quantitated LCAT activity in eleven premature infants maintained on total parenteral nutrition (TPN). Ten infants were studied during the first 2 weeks after birth; they received daily infusions of Intralipid at a rate of 0.5-2.0 g/kg/day over 15 h. One infant received 3.8 g/kg/day during the second week. In addition to LCAT, serum apoprotein A1 (the cofactor of LCAT), cholesterol, triglycerides, and free fatty acids were quantitated. Blood specimens were taken before the start of the infusion and 15-45 min before its completion. The LCAT activity and apoprotein A1 concentrations remained, respectively, 21-24% and 30-35% of adult levels. However, serum cholesterol levels remained in the normal range during the fat infusion. It remains to be established whether low LCAT activity and apoprotein A1 levels are due to the administration of Intralipid (which lowers LCAT activity in rats), to the lack of enteral feedings, or to prematurity per se. Our data suggest that administration of Intralipid at a rate not exceeding 1-2 g/kg/day does not impair the clearing of Intralipid-lecithin and the metabolism of cholesterol.