Leucine Kinetics during Feeding in Normal Newborns

DENNE, SCOTT C.; ROSSI, ELENA M.; Kalhan, Satish C.

doi:10.1203/00006450-199107010-00005

Cited by 22 publications

(25 citation statements)

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“…This is similar to the increase in protein synthesis with enteral feeding previously reported for prepubertal subjects with cystic fibrosis (7) and for newborn infants (25). These results suggest that adolescents with quiescent Crohn disease accomplish protein accretion by increases in protein synthesis and suppression of proteolysis rather than suppression of proteolysis alone.…”

Section: Discussionsupporting

confidence: 74%

“…One participant had a history of treatment with prednisone (10 mg) during the month the study was performed. Crohn disease severity was assessed by using the previously validated Pediatric Crohn's Disease Activity Index (PCDAI), with PCDAI scores categorized as follows: quiescent disease (0 -10), mild disease activity (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), moderate to severe disease activity (Ͼ30) (16). The mean PCDAI was 8 Ϯ 9 [standard deviation (SD)] and range was 0 -25, indicating quiescent to mild disease activity in all subjects at the time of evaluation.…”

Section: Methodsmentioning

confidence: 99%

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Acute Effects of Enteral Nutrition on Protein Turnover in Adolescents with Crohn Disease

et al. 2007

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Adults with inactive Crohn disease have been shown to have normal rates of protein turnover when compared with healthy adults. It is not known whether this is true for adolescents with inactive Crohn disease, when rate of protein synthesis must be greater than that of breakdown for normal development. The objective of this study was to determine whether enteral nutrition acutely suppresses proteolysis and increases protein synthesis in adolescents with inactive Crohn disease. Six adolescents (five males/one female; mean age, 15.8 Ϯ 1.9 y; range, 13.2-17.6 y; mean bone age, 14.6 Ϯ 1.8 y; range, 12.5-17 y) participated. Leucine (Leu) and phenylalanine (Phe) kinetics were measured using stable isotopes under fasted and fed conditions during a single study visit. In response to enteral nutrition, the endogenous rates of appearance (R a ) of Leu and Phe (reflecting proteolysis) decreased significantly by 40%. The percentages of splanchnic uptake of Leu and Phe were 35 Ϯ 10% and 13 Ϯ 12%, respectively. Under fed conditions, utilization of Phe for protein synthesis increased significantly. We conclude that in clinically stable adolescents with Crohn disease, enteral nutrition promotes anabolism by suppressing proteolysis and increasing protein synthesis. Rates of suppression of proteolysis were similar to those reported previously in normal children. (Pediatr Res 61: 356-360, 2007)

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Section: Discussionsupporting

confidence: 74%

Section: Methodsmentioning

confidence: 99%

Acute Effects of Enteral Nutrition on Protein Turnover in Adolescents with Crohn Disease

et al. 2007

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“…With clinical improvement our patients received a higher intake of arginine, and the total arginine flux was higher in convalescent patients compared with that of acute illness. The leucine fluxes, however, were unchanged by the leucine intake and remained within the range of values reported in healthy newborns (21,28). It would appear, then, that diet may have influenced arginine, but not leucine, metabolism.…”

Section: Discussionmentioning

confidence: 66%

Whole Body Arginine Metabolism and Nitric Oxide Synthesis in Newborns with Persistent Pulmonary Hypertension

Castillo

deRojas-Walker

et al. 1995

Pediatr Res

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R A C TDespite the potential relevance of the L-arginine-nitric oxide (NO) pathway in the pathophysiology of pulmonary hypertension, no in vivo studies of the kinetics of arginine and NO have been conducted previously in this population. The terminal guanidino N-atom of L-arginine is the precursor for NO, which is oxidized to the stable inorganic nitrogen oxides, nitrite (NO,-) and nitrate (NO,-). Thus, synthesized NO is detected in serum or urine as NO,-and NO,-. The purpose of this investigation was to compare studies of whole body arginine metabolism twice in nine patients with persistent pulmonary hypertension of the newborn (PPHN), using a primed constant i.v. infusion of ~-[~uanidino-~~N,,5,5~H,]ar~inine and L- [5,5,52~,]leucine, first during acute pulmonary vasoconstriction and again during convalescence, and thereby to characterize quantitative aspects of whole body arginine kinetics and NO production, as estimated from the rate of transfer of the '5~-guanidino-label of arginine to urinary nitrate (ISNO,-). Arginine flux rates were 84.1 ? 8.6 p r n~l -k~. -~h -~ (mean ? SEM) during acute pulmonary hypertension and increased to 125 ? 13.2 ( p < 0.05) during conva-PPHN is an acute vascular maladaptation to extrauterine life, characterized by reactive pulmonary vasoconstriction, causing extrapulmonary shunting of blood across fetal channels and critical hypoxemia. Remodeling of the pulmonary arteries has been observed in some patients with PPHN (1). The etiology of this disorder is uncertain, but a role for altered NO production, a recently discovered key regulator of vascular tone (2-4), Received October 10, 1994; accepted February 27, 1995 Abbreviations PPHN, persistent pulmonary hypertension of the newborn NO, nitric oxide eNOS, nitric oxide synthase AaDO,, alveolo-arterial oxygen gradient ECMO, extracorporeal membrane oxygenation A.P.E., atom percent excess must be considered. NO is produced in the pulmonary and systemic arteries of newborn animals (5) and contributes to the postnatal vasodilation of the pulmonary circulation (6, 7). NO is synthesized in the endothelial cells, through the action of eNOS, and diffuses into subjacent vascular smooth muscle, where it binds to its molecular target, the prosthetic heme group of soluble guanylyl cyclase, forming nitrosyl proteins (8). This process activates guanylyl cyclase, augmenting levels of the second messenger, cGMP (8). Intracellular elevation of cGMP levels activates cGMP-dependent protein kinases, leading to phosphorylation of proteins and inhibition of intracellu-MA 02114. lar calcium release and/or influx through calcium channels.

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“…This high efficiency in the neonate is enabled by an elevated response of protein synthesis to stimulation by feeding (Denne et al, 1991;Burrin et al, 1992;Davis et al, 1996). Although feeding stimulates protein synthesis in all tissues of the neonatal pig, the greatest response occurs in skeletal muscle.…”

Section: Postnatal Ontogeny Of the Feeding-induced Stimulation Of Musmentioning

confidence: 99%

Postnatal ontogeny of skeletal muscle protein synthesis in pigs1,2

Davis

Suryawan

Orellana

et al. 2008

Journal of Animal Science

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The neonatal period is characterized by rapid growth and elevated rates of synthesis and accretion of skeletal muscle proteins. The fractional rate of muscle protein synthesis is very high at birth and declines rapidly with age. The elevated capacity for muscle protein synthesis in the neonatal pig is driven by the high ribosome content and, together with an increased efficiency of the translation process, promotes accelerated protein synthesis rates. Feeding profoundly stimulates muscle protein synthesis in neonatal pigs and the response decreases with age. The feeding-induced stimulation of muscle protein synthesis is modulated by an enhanced sensitivity to the postprandial increase in insulin and amino acids. The developmental decline in the response to insulin and amino acids parallels a marked decrease in the feeding-induced activation of translation initiation factors that regulate the binding of mRNA to the 40S ribosomal complex. The abundance and activation of many known positive regulators of the nutrient-and insulin-signaling pathways that are involved in translation initiation are high, whereas those of many negative regulators are low in skeletal muscle of younger pigs. Thus, the activation and(or) abundance of the positive regulators, such as the insulin receptor, insulin receptor-substrate-1, phosphoinositide-3 kinase, phosphoinositide-dependent kinase-1, protein kinase B, mammalian target of rapamycin, raptor, ribosomal protein S6 kinase-1, eukaryotic initiation factor (eIF) 4E-binding protein 1, and eIF4E associated with eIF4G, are greater in 7-d-old pigs than in 26-d-old pigs. The activation of negative regulators, including protein tyrosine phosphatase-1B, phosphatase and tensin homologue deleted on chromosome 10, protein phosphatase 2A, and tuberous sclerosis complex 1/2, are lower in 7-d-old pigs than in 26-d-old pigs. Thus, the developmental decline in the stimulation of skeletal muscle protein synthesis by insulin and amino acids is due in part to the developmentally related decrease in the activation of the signaling pathways that lead to translation initiation.

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Leucine Kinetics during Feeding in Normal Newborns

Cited by 22 publications

References 0 publications

Acute Effects of Enteral Nutrition on Protein Turnover in Adolescents with Crohn Disease

Acute Effects of Enteral Nutrition on Protein Turnover in Adolescents with Crohn Disease

Whole Body Arginine Metabolism and Nitric Oxide Synthesis in Newborns with Persistent Pulmonary Hypertension

Postnatal ontogeny of skeletal muscle protein synthesis in pigs1,2

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