Feeding of Premature Infants

Gordon, H. McL.

doi:10.1001/archpedi.1947.02020390054002

Cited by 138 publications

(5 citation statements)

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“…Thus, the total amount of milk protein fed to a mammalian neonate correlates to the total leucine uptake provided by milk of the mammalian species and appears to be associated with leucine-mediated growth. These observations are in accordance with premature infants fed formula containing a higher protein concentration who gained weight faster than those fed formulas with a lower protein concentration closer to that of human milk [38]. …”

Section: Total Leucine Uptake By Mammalian Milk and Neonatal Growtsupporting

confidence: 81%

Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity

Melnik

2012

Journal of Obesity

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Increased protein supply by feeding cow-milk-based infant formula in comparison to lower protein content of human milk is a well-recognized major risk factor of childhood obesity. However, there is yet no conclusive biochemical concept explaining the mechanisms of formula-induced childhood obesity. It is the intention of this article to provide the biochemical link between leucine-mediated signalling of mammalian milk proteins and adipogenesis as well as early adipogenic programming. Leucine has been identified as the predominant signal transducer of mammalian milk, which stimulates the nutrient-sensitive kinase mammalian target of rapamycin complex 1 (mTORC1). Leucine thus functions as a maternal-neonatal relay for mTORC1-dependent neonatal β-cell proliferation and insulin secretion. The mTORC1 target S6K1 plays a pivotal role in stimulation of mesenchymal stem cells to differentiate into adipocytes and to induce insulin resistance. It is of most critical concern that infant formulas provide higher amounts of leucine in comparison to human milk. Exaggerated leucine-mediated mTORC1-S6K1 signalling induced by infant formulas may thus explain increased adipogenesis and generation of lifelong elevated adipocyte numbers. Attenuation of mTORC1 signalling of infant formula by leucine restriction to physiologic lower levels of human milk offers a great chance for the prevention of childhood obesity and obesity-related metabolic diseases.

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Section: Total Leucine Uptake By Mammalian Milk and Neonatal Growtsupporting

confidence: 81%

Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity

Melnik

2012

Journal of Obesity

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“…However, as lower leucocyte ascorbic acid levels are also observed in smokers, an increased incidence of smoking in the Iower-birthweight group does not necessarily argue against ascorbic acid as a factor in determining birth weight. On the other hand, nutritional status in later pregnancy should arguably be important in determining the size of the child and multinutritional deficiencies are more likely to be disadvantageous to the foetus than ascorbic acid depletion alone (Dobbing, 1970;Gordon, 1975;Smithells et al 1976).…”

Section: Discussionmentioning

confidence: 99%

Leucocyte ascorbic acid and pregnancy

et al. 1978

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1. Leucocyte ascorbic acid concentrations have been measured in 1147 females during early pregnancy and in smaller numbers of women before conception, throughout pregnancy and at 6 months post partum. 2. The leucocyte concentration in the 1st trimester was found to be affected by season, social class and smoking. Selecting individuals by extremes of social class, season and smoking produced two small populations with almost separate ascorbic acid distributions and mean concentrations of 21.7 and 45.1 microgram/10(8) leucocytes. 3. Early pregnancy had little effect on leucocyte ascorbic acid concentrations but values decreased in the second trimester. However, this was associated with a leucocytosis so that the total leucocyte ascorbic acid content of blood was unchanged. 4. Low ascorbic acid concentrations during the 1st trimester were not associated with subsequent spontaneous abortions, still-births or neonatal deaths, but there was an increased frequency of low values in women who gave birth to infants smaller than 3250 g. 5. The adequacy of ascorbic acid reserves in early pregnancy is discussed.

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“…Postnatal protein administration is essential for growth and recovery of preterm infants (8,37,38); however, aggressive postnatal parenteral amino acid administration has been tempered by concerns about potential toxicity (39). The minimal lipid stores of ELBW infants and the relatively high protein requirements of these infants have prompted reconsideration of the arbitrary limits placed on early postnatal amino acid administration (40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

“…Daily administration of as little as 1.5 g/kg amino acid can prevent endogenous amino acid loss (7). Early studies by Gordon et al (8) showed that low-birth-weight infants who received4g•k g −1 • d −1 or more of protein gained weight more rapidly, con-sistent with estimated third-trimester transplacental amino acid transfer rates (9)(10)(11)(12).…”

mentioning

confidence: 99%

Increased Parenteral Amino Acid Administration to Extremely Low‐Birth‐Weight Infants During Early Postnatal Life

Porcelli,

Sisk

2002

J. pediatr. gastroenterol. nutr.

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BackgroundEarly administration of parenteral amino acids to infants with extremely low birth weight (birth weight ≤1,000 g) has been encouraged to foster growth. However, excessive intravenous intake of amino acids may cause metabolic acidosis and uremia in extremely low birth weight infants. The hypothesis for this study was that extremely low birth weight infants would tolerate slightly increased early postnatal parenteral amino acid administration and benefit.MethodsThe peak daily parenteral amino acid dosage was increased from 3 g/kg (standard group) to 4 g/kg (modified group). The corrected parenteral amino acid dosage was computed to account for enteral protein intake and keep the combined daily intravenous amino acid and enteral protein intake at or below 3 g · kg−1 · d−1 in the standard group and 4 g · kg−1 · d−1 in the modified group. The primary outcome measure was plasma bicarbonate concentration as an indicator of acid–base status. Data were collected for patient demographics, nutritional intake, serum bicarbonate and serum urea nitrogen concentrations, and outcome.ResultsThe corrected parenteral amino acid intake of the modified group was 16% greater at postnatal week 1 (3.30 ± 0.83 g · kg−1 · d−1; mean, ±1 SD) and 18% greater (3.86 ± 0.94 g · kg−1 · d−1) at postnatal week 2 than the parenteral amino acid intake of the standard group. In the modified group, the mean serum bicarbonate concentration was 19.1 ± 1.8 mEq/dL at week 1 and 23.9 ± 2.9 mEq/dL at week 2, with no difference between the groups. At week 1, serum urea nitrogen concentrations were the same in both groups. The mean serum urea nitrogen concentration of the modified group at postnatal week 2 (18.2 ± 8.8 mg/dL) was unchanged from postnatal week 1, but was greater than that of the standard group at postnatal week 2. Weight gain was the same in both groups. Corrected parenteral amino acid intake at postnatal week 1 correlated directly with weight gain from birth to postnatal week 2 (P < 0.03) in both groups.ConclusionsInfants with extremely low birth weight tolerated parenteral amino acid intake of approximately 4 g · kg−1 · d−1. Mild increases of mean serum urea nitrogen concentration and mean weight gain were associated with increased parenteral amino acid administration without significant acidosis.

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Feeding of Premature Infants

Cited by 138 publications

References 12 publications

Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity

Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity

Leucocyte ascorbic acid and pregnancy

Increased Parenteral Amino Acid Administration to Extremely Low‐Birth‐Weight Infants During Early Postnatal Life

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