Lecithin-cholesterol acyltransferase in newborn infants: Low activity level in preterm infants

Papadopoulos, Andrea; Hamosh, Margit; Chowdhry, Parveen; Scanlon, John W.; Hamosh, Paul

doi:10.1016/s0022-3476(88)80027-1

Cited by 20 publications

(14 citation statements)

References 13 publications

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“…In addition, HDL and other lipoproteins and apo synthesized in the intestine during fat absorption may affect LCAT activity (27) and could explain the differences in the cholesterol esterification observed, Another finding in this study may be related to lipid tolerance in preterm infants. A lower capacity for cholesterol esterification at birth and during the early postnatal age in preterm infants has been reported (23,(29)(30)(31). The preterm infants who received nucleotides showed a proportion of plasma cholesterol-esters close to that found in term infants, whereas this proportion remained low in the group fed the nucleotide-free formula.…”

Section: Discussionmentioning

confidence: 72%

Dietary Nucleotides Influence Lipoprotein Metabolism in Newborn Infants

et al. 1994

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ABSTRACT. Nucleotide supplementation of adapted-milk formulas may be of interest for infant nutrition because nucleotides are involved in the synthesis of proteins and other macromolecules such as phospholipids, and thereby facilitate lipoprotein synthesis. To determine whether dietary nucleotides influence plasma lipoproteins in newborns, we have studied the plasma-lipoprotein concentrations and the composition of the major lipoprotein fractions during the first week of life in two groups of preterm infants fed formulas differing only in their nucleotide content. For comparison, two groups of term infants were studied under the same conditions. Lipoproteins were isolated by density ultracentrifugation, and the lipid and protein content were determined by standard methods; apolipoprotein A-I was determined immunologically. Nucleotide supplementation of formula in preterm infants increased all plasma lipoprotein concentrations. In addition, an increase in the plasma esterification rate was observed. However, total cholesterol concentrations were unchanged. The changes in lipoproteins concentrations were due mainly to an increase in apolipoprotein content. Nucleotides added to formulas affected term-infants' lipoproteins significantly less than to perterm infants. These findings suggest that dietary nucleotides may enhance the synthesis of lipoproteins during the early neonatal period, especially in preterm infants. 35: 112-116,1994) Abbreviations LCAT, lecithin/cholesterol-acyl transferase CMP, cytidine monophosphate UMP, uridine monophosphate IMP, inosine monophosphate PTI-NFF, preterm infants fed nucleotide-free formula PTI-NSF, preterm infants fed nucleotide-supplemented formula TI-NFF, term infants fed nucleotide-free formula TI-NSF, term infants fed nucleotide-supplemented formula Nucleotides are present in most food products as nucleic acids from which nucleotides are released after digestion (1). Nucleic acids as well as free nucleotides are found in human milk in significant amounts (2, 3), and the nutritional role of these components is currently under study. Dietary nucleotides seem to influence several aspects of neonatal development (4-9), but little is known about the influence of nucleotides in lipoprotein (Pcdiatr Rcs

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Section: Discussionmentioning

confidence: 72%

Dietary Nucleotides Influence Lipoprotein Metabolism in Newborn Infants

et al. 1994

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“…18 Early studies showed that HDL 2 and HDL 3 cholesterol concentrations and LCAT activity are lower at birth in full term infants than in adults. 19 20 We have reported previously that LCAT activity is low in small for gestational age newborns. 21 However, no information has been provided on HDL subfractions and LCAT activity in the sera of macrosomic infants of diabetic mothers.…”

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confidence: 94%

Fetal macrosomia related to maternal poorly controlled type 1 diabetes strongly impairs serum lipoprotein concentrations and composition

Merzouk

Bouchenak²,

Loukidi³

et al. 2000

Journal of Clinical Pathology

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Aims-To determine the eVects of fetal macrosomia related to maternal type 1 diabetes on the lipid transport system. Methods-Serum lipoprotein concentrations and composition and lecithin:cholesterol acyltransferase (LCAT) activity were investigated in macrosomic newborns (mean birth weight, 4650 g; SEM, 90) and their mothers with poorly controlled type 1 diabetes, in appropriate for gestational age newborns (mean birth weight, 3616 g; SEM, 68) and their mothers with well controlled type 1 diabetes, and macrosomic (mean birth weight, 4555 g; SEM, 86) or appropriate for gestational age (mean birth weight, 3290 g; SEM, 45) newborns and their healthy mothers. Results-In mothers with well controlled type 1 diabetes, serum lipids, apolipoproteins, and lipoproteins were comparable with those of healthy mothers. Similarly, in their infants, these parameters did not diVer from those of appropriate for gestational age newborns. Serum triglyceride, very low density lipoprotein (VLDL), apolipoprotein B100 (apo B100), and high density lipoprotein (HDL) triglyceride concentrations were higher, whereas serum apo A-I and HDL 3 concentrations were lower in mothers with diabetes and poor glycaemic control than in healthy mothers. Their macrosomic newborns had higher concentrations in all serum lipids and lipoproteins, with high apo A-I and apo B100 values compared with appropriate for gestational age newborns. In macrosomic infants of healthy mothers, there were no significant diVerences in lipoprotein profiles compared with those of appropriate for gestational age infants. LCAT activity was similar in both groups of mothers and newborns. Conclusion-Poorly controlled maternal type 1 diabetes and fetal macrosomia were associated with lipoprotein abnormalities. Macrosomic lipoprotein profiles related to poor metabolic control of type 1 diabetes appear to have implications for later metabolic diseases. (J Clin Pathol 2000;53:917-923)

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“…Indeed, LCAT activity was found to be lower at birth than in adults (9)(10)(11)(12). Therefore, attempts to understand the mechanism(~) involved in lipid clearing and particularly the regulatory factors of LCAT activity, have been made (10,(13)(14)(15)(16).…”

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confidence: 99%

Low Levels of Apolipoprotein A1 Are Not Contributors to the Low Lecithin-Cholesterol Acyl Transferase Activity in Premature Newborn Infants

et al. 1988

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ABSTRACT. Umbilical cord sera were obtained from three groups of newborn infants; group I ((n = 8) and group I1 (n = 12) weighed less than 1500 g and between 1500 and 2500 g, respectively. Group 111 (n = 16) was full term and weighed more than 2500 g. Lecithin-cholesterol acyl transferase activities, determined as the rates of esterification of [3Hjcholesterol, were 0.13 f 0.01,0.17 f 0.01, and 0.26 f 0.01 (mean SEM) nmol/h/ml for groups I, 11, and 111, respectively. The adult value (n = 8) was 0.96 f 0.01 nmol/h/ml. The respective apolipoprotein A1 (apo-A,) levels were 52 2 6, 59 f 4, and 67 f 4 (mean f SEM) mg/ dl. Serum level of apo-Al in adults was 137 f 6 mg/dl. Plasma high-density lipoprotein cholesterol levels increased with gestational age. However, in newborn infants, high-density lipoprotein apo-lipoprotein B, total cholesterol, and triglyceride levels, were significantly lower than in adults. These data indicate that serum levels of lecithincholesterol acyl transferase activity significantly (p < 0.01) increase whereas the levels of apo-A, do not significantly change with the gestational age. Also, in full-term newborns, lecithin-cholesterol acyl transferase activity is only 27'70, whereas apo-A1 levels are 49% of adult values. Therefore, lower levels of apo-A1 do not account for the significantly lower activity of lecithin-cholesterol acyl transfierase in preterm as compared to full-term newborn infants. (Pediatr Res 24: 191-193, 1988) Abbreviations LCAT, lecithin-cholesterol acyl transferase Apo-A,, apolipoprotein Al HDL, high-density lipoprotein Apo-El, apolipoprotein B LCAT is an enzyme that converts plasma lecithin and unesterified cholesterol to lysolecithin and cholesteryl ester, and therefore, it plays a key role in the metabolism of phospholipids (1, 2). The latter, as one of the components of fat emulsions, is commonly administered to low birth weight premature infants, who are maintained on total parenteral nutrition. In these new-

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Lecithin-cholesterol acyltransferase in newborn infants: Low activity level in preterm infants

Cited by 20 publications

References 13 publications

Dietary Nucleotides Influence Lipoprotein Metabolism in Newborn Infants

Dietary Nucleotides Influence Lipoprotein Metabolism in Newborn Infants

Fetal macrosomia related to maternal poorly controlled type 1 diabetes strongly impairs serum lipoprotein concentrations and composition

Low Levels of Apolipoprotein A1 Are Not Contributors to the Low Lecithin-Cholesterol Acyl Transferase Activity in Premature Newborn Infants

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