摘要:

Our goal for this study was to determine whether the maturation of fat absorption in neonatal life is functionally related to an increased ability to hydrolyze dietary fat, to absorb long-chain fatty acids, or to do both. In 16 preterm and in eight term neonates, the intestinal ability to hydrolyze triacylglycerols and the capacity to absorb long-chain fatty acids were determined at several times between birth and 5 mo after the term age. These processes were compared with the percentage of fat absorption (formula-fed infants) or with fecal fat excretion (breast-fed infants). The functional capacity to digest triacylglycerols and to absorb the lipolytic products was evaluated by measuring serum concentrations of the lipolytic product [1-13C]palmitate after the enteral administration of tri-1-13C palmitoyl-glycerol. Long-chain fatty acids absorption (i.e.independent of lipolysis) was determined by measuring serum concentrations of [1-13C]stearate after its enteral administration. The efficacy of fat absorption increased in preterm infants (formula-fed) from 91.2 ± 1.1% (mean ± SEM) at 32.3 wk postconceptional age (PCA) to 97.3 ± 0.6% at 53.6 wk PCA (p< 0.001), and in term infants from 91.7 ± 1.8% (40.0 wk PCA) to 97.4 ± 1.3% (58.9 wk PCA,p= 0.07). Both the serum concentration of [1-13C]stearate and that of [1-13C]palmitate appeared highly correlated with the efficacy of fat absorption (r= 0.82,p= 0.02; andr= 0.91,p= 0.004; respectively) and with PCA (r= 0.99,p< 0.001; andr= 0.85,p< 0.02; respectively). These results indicate that the functional development of fat absorption in preterm and term infants is related to the capacity to absorb long-chain fatty acids from the intestine.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Immaturity of intestinal epithelial barrier function and absorptive capacity may play a role in the pathophysiology of intestinal complications in preterm neonates during the early postnatal period. We determined the intestinal permeability and carrier-mediated absorption of monosaccharides in preterm neonates during the first 2 wk after birth. Fifty-nine preterm neonates born between 25 and 32 wk gestation were included within 24 h of birth. Neonates received exclusively parenteral nutrition during the first 7 d after birth; enteral feeding was initiated at d 8. An intestinal permeability-absorption test was performed at 1, 4, 7, and 14 d after birth. The lactulose-to-rhamnose ratio was determined as a marker of intestinal permeability. Urinary excretion percentages of d-xylose and 3-O-methyl-d-glucose were determined as markers of passive and active carrier-mediated monosaccharide absorption, respectively. Intestinal permeability transiently increased between d 1 and 7 in all neonates (p< 0.05). Carrier-mediated monosaccharide absorption increased between d 1 and 14 in neonates of 28–30 wk (p< 0.05) to the level observed in the neonates of 30–32 wk gestation. In neonates <28 wk, intestinal permeability at d 7 was higher (p< 0.05) and carrier-mediated monosaccharide absorption at d 14 was lower (p< 0.01) as compared with neonates ≥28 wk. The barrier function of the intestinal epithelium transiently decreases during the first week after birth in preterm neonates who are not enterally fed. Diminished barrier function and low monosaccharide absorptive capacity, particularly in neonates <28 wk, may predispose these patients to the development of intestinal complications during the early postnatal period.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The inorganic selenium compounds selenite and selenate are used for selenium fortification of infant formulas. However, information on absorption and retention of selenium from these compounds is lacking. The purpose of this study was therefore to determine apparent absorption and retention of selenium from selenate and selenite added to a milk-based infant formula in healthy infants. Labeled test meals were prepared by addition of 10 &mgr;g Se as76Se-selenate or74Se-selenite to 500 mL formula. The two batches of labeled formulas were fed as alternate feeds during the first day of the balance period, followed by unlabeled formula. Selenium isotopes were determined in feces collected for 72h after intake and in 3 consecutive 24h collections of urine. Mean apparent absorption was 97.1% for76Se-selenate and 73.4% for74Se-selenite; mean difference 23.7% (range: 13.8%–35.7%; SD 6.8%,p< 0.001). Mean urinary excretion (% of ingested dose) was 36.4% (76Se-selenate) and 9.7% (74Se-selenite); mean difference 26.7% (range: 13.9%–36.5%; SD 5.9%,p< 0.001). Mean apparent retention of selenium from76Se-selenate and74Se-selenite was not significantly different, 60.7% (76Se-selenate)versus63.7% (for74Se-selenite). The average difference was −3.01% (range: −14.0%–12.0%; SD 9.4%,p= 0.36). Although apparent selenium absorption and urinary excretion differed for selenite and selenate, selenium was equally well retained by infants from both selenium compounds. We therefore concluded that Se fortification of infant formulas with selenate or selenite can be expected to have similar impact on the selenium nutritional status of term infants.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

To determine whether hyperinsulinemia and reduced insulin sensitivity in individuals born small for gestational age (SGA) could be related to persisting abnormalities of the GH/IGF-I axis, we assessed overnight GH secretory profiles and measured fasting glucose, insulin, intact and 32,33 split proinsulin, and IGF-I levels in 16 short SGA children (age range 2.3–8.0 y) and in controls. Insulin sensitivity was calculated using the homeostasis model. Compared with short normal-birthweight controls (n= 7, age range 2.3–5.0 y), short SGA children had higher fasting insulin levels (means: 26.8vs20.6 pmol/L,p= 0.02), lower insulin sensitivity [means: 204vs284 %homeostasis model assessment (HOMA),p= 0.01], and higher beta cell function (112vs89 %HOMA,p= 0.04). SGA children also had lower levels of IGFBP-1 (87.0vs133.8,p= 0.04), but similar IGF-I levels (IGF-I SDS: -1.1vs-1.7,p= 0.4). Compared with normal-height controls (n= 15, age range 5.6–12.1 y), SGA children had higher overnight GH secretion (GH maximum: 55.9vs39.6 mU/L,p= 0.01; mean: 13.1vs8.9,p= 0.004; minimum: 1.2vs0.6,p= 0.02). Interestingly, among SGA children, fasting insulin levels and insulin sensitivity were significantly related to overnight GH secretion (insulin sensitivityvsmaximum GH: r = −0.68,p= 0.01;vsGH pulse amplitude r = −0.71,p= 0.007). The only hormone level significantly related to current height velocity was C-peptide (r = 0.75,p= 0.008). In conclusion, elevated fasting insulin levels and reduced insulin sensitivity in short SGA children was related to elevated levels of overnight GH secretion. We hypothesize that resistance to the somatotropic actions of GH and IGF-I in short SGA children may contribute directly to reduced insulin sensitivity.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The cause of skeletal muscle insulin resistance is unclear, but high levels of intramyocellular lipids are often present in affected individuals. We aimed to establish the metabolic, familial, and anthropometric associations of intramyocellular lipid in a pediatric population. We studied 41 boys aged 6.9–9.9 y and 23 of their mothers by proton magnetic resonance spectroscopy. We related muscle lipid levels to important factors that define an increased risk of developing insulin resistance in adult life. There were significant associations between the boys’ intramyocellular lipid and their waist circumference (r = 0.42,p= 0.007), body mass index SD score (r = 0.32,p= 0.04), weight SD score (r = 0.32,p= 0.04), glucose:insulin ratio (r=−0.59,p= 0.04), maternal log fasting insulin levels (r = 0.44,p= 0.04), maternal body mass index (r = 0.46,p= 0.03), and maternal intramyocellular lipid (r = 0.62,p= 0.003). In the 41 boys, waist circumference explained 19% of the variance in the boys’ intramyocellular lipid. Maternal intramyocellular lipid explained 39% of the variance in the boys’ intramyocellular lipid in the sub-group of 23 boys. Intramyocellular lipid levels have both metabolic and anthropometric associations in childhood. Before puberty, children develop or inherit muscle metabolic characteristics that are associated both with insulin resistance and risk factors for the development of insulin resistance syndrome in adult life.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Although very low birth weight infants are subjected to severe stress and glutamine is now considered a conditionally essential amino acid that may attenuate stress-induced protein wasting in adults, current amino acid solutions designed for neonatal parenteral nutrition do not contain glutamine. To determine whether a short-term supplementation with i.v. glutamine would affect protein metabolism in very low birth weight infants, 13 preterm neonates (gestational age, 28–30 wk; birth weight, 820–1610 g) receiving parenteral nutrition supplying 1.5 g · kg−-1· d−1amino acids and approximately 60 nonprotein kcal · kg−1· d−1were randomized to receive an i.v. supplement made of either1) natural l-glutamine (0.5 g · kg−1· d−1; glutamine group), or2) an isonitrogenous glutamine-free amino acid mixture (control group), for 24 h starting on the third day of life. On the fourth day of life, they received a 2-h infusion of NaH13CO3to assess the recovery of13C in breath, immediately followed by a 3-h l-[1-13C]leucine infusion. Plasma ammonia did not differ between the groups. Glutamine supplementation was associated with1) higher plasma glutamine (629 ± 94versus503 ± 83 &mgr;M, mean ± SD;p< 0.05, one-tailed unpairedttest),2) lower rates of leucine release from protein breakdown (−16%,p< 0.05) and leucine oxidation (−35%,p< 0.05),3) a lower rate of nonoxidative leucine disposal, an index of protein synthesis (−20%,p< 0.05), and4) no change in protein balance (nonoxidative leucine disposal − leucine release from protein breakdown, NS). We conclude that although parenteral glutamine failed to enhance rates of protein synthesis, glutamine may have an acute protein-sparing effect, as it suppressed leucine oxidation and protein breakdown, in parenterally fed very low birth weight infants.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Intrauterine growth retardation (IUGR) is one of the major causes of short stature in childhood. Although postnatal catch-up growth occurs in the majority of IUGR children, approximately 20% of them remain permanently short. The mechanisms that allow catch-up growth or, on the contrary, prevent IUGR children from achieving a normal height are still unknown. Our aim was to investigate whether intrauterine reprogramming of hypothalamic-pituitary-adrenal axis may be involved in postnatal growth retardation of IUGR children through a modulation of the function of the IGF system. Anthropometry, IGF system assessment, cortisol measurement, and lipid profile evaluation were performed in 49 IUGR children. Children were subdivided into two groups according to their actual height corrected for midparental height: CG (catch-up growth) group, 19 children with corrected height ≥0 z-score; and NCG (noncatch-up growth) group, 30 subjects with corrected height <0 z-score. CG children showed significantly higher birth weight (p< 0.005) and body mass index (p< 0.05). No significant differences in IGF-I, IGF-II, IGF binding protein (IGFBP)-1, IGFBP-3, soluble IGF-II receptor levels (IGF2R), IGF-II/IGF2R ratio, and relative amounts of IGFBP-3 circulating forms were found between CG and NCG children. None of the IGF system-related variables correlated with anthropometric indices. NCG children showed significantly higher concentrations of cortisol (p< 0.005) and cortisol levels resulted inversely to birth weigh (r= −0.34,p< 0.05), birth length (r= −0.36,p< 0.05), and corrected height (r= −0.44,p< 0.01). Whereas total and HDL cholesterol concentrations were not significantly different in the two groups, LDL cholesterol levels were significantly higher in NCG children (p< 0.05), and five of 49 showed LDL cholesterol concentrations >3.4 mM (130 mg/dL). LDL cholesterol was inversely related to birth weight (r= −0.31,p< 0.05), corrected stature (r= −0.32,p< 0.05), and actual height (r= −0.31,p< 0.05) and directly related to the levels of IGF2R (r= 0.44,p< 0.01). Reanalysis of 15 of 30 IUGR newborns in whom we previously reported an inverse relationship between cord blood cortisol levels and first trimester length gain (r= −0.54,p< 0.005) showed that the relative amount of the IGFBP-3 18-kD fragment was related inversely to cortisol (r= −0.67,p< 0.01) and directly to early postnatal growth (r= 0.65,p< 0.05). Our results suggest that catch-up growth in IUGR children might be affected by intrauterine reprogramming of hypothalamic-pituitary-adrenal axis, which may result in a permanent modification of the neuroendocrine response to stress: children with increased cortisol secretion may be at higher risk of growth failure. During the neonatal period cortisol might act by limiting IGFBP-3 proteolysis and, therefore, reducing IGF bioavailability.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The relationship between skin color and illness severity in the newborn remains untested. We have evaluated the predictive value of skin color readings for illness severity in a population of high-risk newborn infants. A prospective study was conducted on 107 white newborns in the intensive care unit, which were categorized as either high or low severity of illness, defined by the presence of severe neonatal morbidity. Illness severity was also determined using a Score for Neonatal Acute Physiology (SNAP). Color readings were obtained at 10 different body sites using a portable tristimulus colorimeter during the first 24 h, and color was expressed using the standard CIE L*a*b* system. Skin CIE b* values were significantly lower in the high severity group (p< 0.0001), and a significant inverse correlation with SNAP was observed (rsrange, −0.37 to −0.71,p< 0.0001). In particular a low b* value for the abdomen was found to be a significant predictor of illness severity (92.6% sensitivity; 96.6% specificity; 96% positive predictive value; 93.7% negative predictive value; adjusted odds ratio, 14.7; 95% confidence interval, 6.4 to 33.8). Our findings indicate that skin color reflects clinical severity in the newborn and that skin colorimetry can accurately identify higher risk infants.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The C protein &agr;- and &bgr;-antigens are immunodominant components of the surface ofStreptococcus agalactiae, the most frequent cause of neonatal sepsis. Both proteins are thought to contribute significantly to virulence ofS. agalactiae. They are mainly expressed by serotypes Ia, Ib, and II. The C protein &bgr;-antigen (C&bgr;-protein) binds to the Fc portion of human IgA and seems to be of importance in bacterial resistance to mucosal immune defense mechanisms. In this study, PCR analysis ofS. agalactiaeisolates obtained from 189 neonates and 112 pregnant women revealed the presence of the C&bgr;-protein gene in 19% and 22% of the isolates, respectively. Size polymorphisms of the PCR products within the gene region encoding the cell wall–spanning domain indicated a high degree of genetic variability. Thirteen different variants of the amplified region were differentiated among the 60 C&bgr;-protein–positive isolates by sequence analysis. In all variants, the polymorphisms were caused by insertions and deletions of repetitive DNA elements that did not alter the open reading frame. Comparison of the C&bgr;-protein gene polymorphisms showed a significantly higher rate of isolates carrying deletions >50 bp in serotype Ib than in serotype II isolates (p= 0.001); this was also true for neonatal isolates analyzed separately (p= 0.01). Neonatal isolates carried a higher rate of large deletions when compared with maternal isolates; this difference, however, did not reach statistical significance (p= 0.08). We hypothesize that polymorphisms in the cell wall–spanning domain of the C&bgr;-protein are of functional relevance with regard to maternofetal transmission of the pathogen.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The pathogenesis of bilirubin encephalopathy appears to result from accumulation of unconjugated bilirubin (UCB), which, in turn, may cause mitochondrial perturbation, release of intermembrane proteins, and, ultimately, cell death. Aging imparts to cells a different susceptibility to this toxic stimulus, as neonates are particularly vulnerable to the accumulation of UCB in the CNS. In this paper, we further characterize UCB-induced toxicity in isolated neuronal and glial cells according to age in culture. In addition, we investigate sensitivity of mitochondria derived from young and old rats to UCB-induced membrane permeabilization and, finally, evaluate whether age-dependent changes in UCB toxicity are accompanied by alterations in the mitochondrial content of cytochromec. The results showed that UCB is more toxic to immature neural cells after 4–5 d in culture (p< 0.001), whereas neurons were more sensitive than astrocytes (p< 0.05). In fact, approximately 40% of cells were apoptotic in immature cultures compared with 20% in mature cultures. Unexpectedly, mitochondrial swelling and subsequent efflux of cytochromecinduced by UCB were 2-fold greater in organelles derived from older rats (p< 0.01). In conclusion, UCB toxicity of isolated rat neuronal and glial cells is modulated by age in culture in that immature cells are more susceptible. Mitochondria derived from younger rats are nevertheless more resistant to membrane permeabilization and cytochromecrelease induced by UCB. The data indicate that the cells of young animals are relatively resistant to UCB toxicity, through a protective mechanism at the mitochondrial level; however, this is not sufficient to prevent apoptosis of cells in the young animal. Thus, although playing a role, direct mitochondrial injury may not be the sole mechanism of UCB cytotoxicity.

ISSN:0031-3998    

出版商:OVID    

年代:2002

数据来源: OVID