Parenteral nutrition in preterm neonates with and without carnitine supplementation

Larsson, L. E.; Olegård, R; Ljung, Britt Mari; Niklasson, Anna; Rubensson, Allan; Cederblad, G.

doi:10.1111/j.1399-6576.1990.tb03132.x

Cited by 14 publications

(9 citation statements)

References 19 publications

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“…The normative levels and postnatal changes in plasma carnitine in the preterm neonate are now well characterized [36], [37], [38]. Sick preterm neonates who do not receive carnitine supplementation via the enteral or parenteral route continue to have lower tissue carnitine levels [39], [40], [41], [42] which drop further, and thus may develop a state of relative tissue carnitine deficiency. We hypothesize that tissue carnitine deficiency will have an impact at the molecular level in the developing GI tract.…”

Section: Introductionmentioning

confidence: 99%

Carnitine Deficiency in OCTN2−/− Newborn Mice Leads to a Severe Gut and Immune Phenotype with Widespread Atrophy, Apoptosis and a Pro-Inflammatory Response

et al. 2012

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We have investigated the gross, microscopic and molecular effects of carnitine deficiency in the neonatal gut using a mouse model with a loss-of-function mutation in the OCTN2 (SLC22A5) carnitine transporter. The tissue carnitine content of neonatal homozygous (OCTN2−/−) mouse small intestine was markedly reduced; the intestine displayed signs of stunted villous growth, early signs of inflammation, lymphocytic and macrophage infiltration and villous structure breakdown. Mitochondrial β-oxidation was active throughout the GI tract in wild type newborn mice as seen by expression of 6 key enzymes involved in β-oxidation of fatty acids and genes for these 6 enzymes were up-regulated in OCTN2−/− mice. There was increased apoptosis in gut samples from OCTN2−/− mice. OCTN2−/− mice developed a severe immune phenotype, where the thymus, spleen and lymph nodes became atrophied secondary to increased apoptosis. Carnitine deficiency led to increased expression of CD45-B220+ lymphocytes with increased production of basal and anti-CD3-stimulated pro-inflammatory cytokines in immune cells. Real-time PCR array analysis in OCTN2−/− mouse gut epithelium demonstrated down-regulation of TGF-β/BMP pathway genes. We conclude that carnitine plays a major role in neonatal OCTN2−/− mouse gut development and differentiation, and that severe carnitine deficiency leads to increased apoptosis of enterocytes, villous atrophy, inflammation and gut injury.

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Section: Introductionmentioning

confidence: 99%

Carnitine Deficiency in OCTN2−/− Newborn Mice Leads to a Severe Gut and Immune Phenotype with Widespread Atrophy, Apoptosis and a Pro-Inflammatory Response

et al. 2012

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“…Using the keywords ''Clinical Trial'' and ''Carnitine'' to search Medline and the Cochrane Database and our our own personal files we found ten randomized clinical trials [8][9][10][11][12][13][14]16,18,19 (Table 5) (s)). 23,24 Whereas three studies showed improved short-term growth, 13,14,24 none of the three published long-term studies 16,18,19 showed any effect of carnitine on growth.…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10][11][12][13][14] However, one study using high doses, 300 mmol/kg/day, 15 of L-carnitine supplementation showed increased protein oxidation and decreased weight gain. In 2000, only one randomized controlled study had evaluated the effect of long-term use of carnitine on growth in VLBW infants, 16 and this study had been conducted without sample size analysis.…”

Section: Introductionmentioning

confidence: 99%

Lack of Effect of L-Carnitine Supplementation on Weight Gain in Very Preterm Infants

et al. 2005

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Carnitine transfer across the placenta occurs predominantly during the third trimester. Unless L-carnitine is provided, very preterm infants develop carnitine deficiency. Although breast milk and infant formulas contain L-carnitine, parenteral nutrition solutions do not routinely provide L-carnitine. We hypothesized that prolonged L-carnitine supplementation in very preterm infants would improve weight gain and shorten length of stay in the hospital. STUDY DESIGNThe study was a double-blind parallel placebo-controlled randomized clinical trial. Eligible patients were <29 weeks of gestation, <72 hours of age, and did not have a potentially life-threatening congenital malformation or hereditary metabolic disorder. Patients were stratified by gestational age (23 to 25 6/7 and 26 to 28 6/7 weeks), and randomized to receive, either L-carnitine at a dose of 50 mmol/kg/day, or placebo. Carnitine was provided intravenously until the infants tolerated 16 ml/day of feeds. The sample size was calculated to have 80% power to detect a 10% increase in weight gain from birth until 36 weeks of postmenstrual age or discharge from the hospital. Secondary outcome variables included food efficiency (defined as weight gain divided by caloric intake), weight gain at 4 weeks of age, time to regain birth weight and length of stay. RESULTSAmong the 63 infants enrolled in the trial, 32 were randomized to L-carnitine and 31 to placebo. L-Carnitine supplementation did not significantly affect average daily weight gain from birth until 36 weeks or hospital discharge, or any of the secondary outcome variables. CONCLUSIONProlonged supplementation of L-carnitine did not improve long-term weight gain in very preterm infants.

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“…Improved fatty acid oxidation has been demonstrated if the parenteral nutrition solution is supplemented with L-carnitine. [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] Thus the higher LLM index, particularly following the introduction of Intralipid, may reflect a relative carnitine deficiency.…”

Section: Fig 2 Scattergram Of All Llm Index Values (Il and Non-il) mentioning

confidence: 99%

Lipid-laden macrophages in the tracheal aspirate of ventilated neonates receiving Intralipid�: A pilot study

et al. 1999

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Lipid‐laden macrophages (LLM) in tracheal aspirates are reported to be pathognomonic findings in exo‐ and endogenous lipoid pneumonia in adults. A pilot study was carried out to evaluate the effect of lipid infusion on the LLM index of the tracheal aspirates from ventilated neonates. All intubated infants were eligible for the study. Infants receiving parenteral nutrition had intravenous (IV) lipid introduced by 4–7 days of age; most samples after 7 days were from infants receiving IV lipid. Four infants received minimal gastric feeding; none had evidence of aspiration pneumonia. Tracheal aspirates from 28 infants were analyzed for the LLM index. Alveolar macrophages were graded 0–4 in direct relation to the amount of lipid per cell. One hundred macrophages were graded; the maximum possible LLM index was 400. Two hundred forty‐five of 387 tracheal aspirate samples were acceptable for analysis. LLM indices increased during the first week after birth; the mean LLM index then continued in the same range, but with a wide distribution of individual values. The mean LLM index from infants receiving an IV lipid infusion during days 4–7 was 87.9 (SD = 44.8), and was significantly higher compared to 58.7 (SD = 40.8) in infants receiving no IV lipid (P < 0.003). Tracheal aspirates from infants with and without IV lipid infusion yielded many LLM index values >100. These observations invalidate the use of the LLM index >100 as proof of aspiration pneumonia in this group of infants. Pediatr Pulmonol. 1999; 28:101–108. © 1999 Wiley‐Liss, Inc.

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Parenteral nutrition in preterm neonates with and without carnitine supplementation

Cited by 14 publications

References 19 publications

Carnitine Deficiency in OCTN2−/− Newborn Mice Leads to a Severe Gut and Immune Phenotype with Widespread Atrophy, Apoptosis and a Pro-Inflammatory Response

Carnitine Deficiency in OCTN2−/− Newborn Mice Leads to a Severe Gut and Immune Phenotype with Widespread Atrophy, Apoptosis and a Pro-Inflammatory Response

Lack of Effect of L-Carnitine Supplementation on Weight Gain in Very Preterm Infants

Lipid-laden macrophages in the tracheal aspirate of ventilated neonates receiving Intralipid�: A pilot study

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