Carnitine deficiency in premature infants receiving total parenteral nutrition: effect of L-carnitine supplementation. Parenteral nutrition in preterm neonates with and without carnitine supplementation Plasma and tissue levels of lipids, fatty acids and plasma carnitine in neonates receiving a new fat emulsion Effects of high carnitine supplementation on substrate utilization in low-birth-weight infants receiving total parenteral nutrition. Role of L-carnitine in apnea of prematurity: a randomized, controlled trial. Clinical effects of L-carnitine supplementation on apnea and growth in very low birth weight infants. Are Bilirubin and Plasma Lipid Profiles of Premature Infants Dependent on the Lipid Emulsion Infused? Potential inhibitory effects of L-carnitine supplementation on tissue advanced glycation end products in patients with hemodialysis. Effect of Supplementing Pregnant and Lactating Mothers With n-3 Very-Long-Chain Fatty Acids on Children's IQ and Body Mass Index at 7 Years of Age Lack of Effect of L-Carnitine Supplementation on Weight Gain in Very Preterm Infants Carnitine supplementation in premature neonates: effect on plasma and red blood cell total carnitine concentrations, nutrition parameters and morbidity. Demographic and nutritional factors associated with prolonged cholestatic jaundice in the premature infant Nutritional effects of carnitine supplementation in hemodialysis patients. Effects of carnitine supplementation on flow-mediated dilation and vascular inflammatory responses to a high-fat meal in healthy young adults. l-Carnitine Supplementation to Diet: A New Tool in Treatment of Nonalcoholic Steatohepatitis—A Randomized and Controlled Clinical Trial Effects of L-carnitine supplementation on respiratory distress syndrome development and prognosis in premature infants: A single blind randomized controlled trial. Fatty acid profiles, antioxidant
status, and growth of preterm infants fed diets without or with
long-chain polyunsaturated fatty acids
To investigate whether L-carnitine supplementation may correct nutritional carnitine deficiency and associated metabolic disturbances in premature infants receiving total parenteral nutrition , an intravenous fat tolerance test ( 1 gm/kg Intralipid over four hours ) was performed in 29 premature infants 6 to 10 days of age ( 15 receiving carnitine supplement 10 mg/kg . day L-carnitine IV , and 14 receiving no supplement ) .  Total carnitine plasma values were normal or slightly elevated in supplemented but decreased in nonsupplemented infants . In both groups , fat infusion result ed in an increase in plasma concentrations of triglycerides , free fatty acids , D-beta-hydroxybutyrate , and short-chain and long-chain acylcarnitine , but total carnitine values did not change . After fat infusion , the free fatty acids/D-beta-hydroxybutyrate ratios were lower and the increase of acylcarnitine greater in supplemented infants of 29 to 33 weeks ' gestation than in nonsupplemented infants of the same gestational age . This study provides evidence that premature infants of less than 34 weeks ' gestation requiring total parenteral nutrition develop nutritional carnitine deficiency with impaired fatty acid oxidation and ketogenesis .  Carnitine supplementation improves this metabolic disturbance The effects of carnitine supplementation on fat and glucose metabolism and carnitine balance were studied in 12 preterm neonates receiving full or partial parenteral nutrition ( PN ) for 5 to 21 days . The gestational age ranged from 27 to 32 weeks and the birth weight from 790 to 2090 g. The neonates were assigned at r and om to receive either L‐carnitine 10 mg/kg ( n=6 ) or saline ( n=6 ) . In the carnitine group , increased concentrations in plasma of total and free carnitine were observed . Less than 50 % of the given dose was recovered in urine . In the placebo group no changes in the total plasma carnitine concentration were seen . In all neonates plasma triglycerides , free fatty acids , glycerol , alanine , 3‐hydroxybutyrate ( BOB ) , glucose and lactate were measured at predetermined intervals . The only significant difference between the groups was higher BOB‐concentrations in the carnitine group 2 days after the start of parenteral nutrition . Elevated BOB concentrations are an indicator of improved fatty acid oxidation in the carnitine group . In this study , only a temporary effect of the carnitine supplementation was found This study was undertaken to compare Intralipid ® with a new fat emulsion containing gamma‐linolenic acid and carnitine , named Pediatric Fat Emulsion 4501 , in neonates with regard to lipid and carnitine metabolism over a short period of total parenteral nutrition . There were 10 neonates in each group and they tolerated the total parenteral nutrition well . In spite of the gamma‐linolenic acid supplementation in the new emulsion , arachidonic acid decreased significantly in plasma lipid esters and adipose tissue in both groups after 5 d of treatment . Also , there was a decrease in plasma docosahexaenoic acid which was more pronounced in the treatment group . The relative percentage values of linoleic and linolenic acids in adipose tissue were increased , indicating that newborns have a rapid accretion of fatty acids . Plasma triglycerides were effectively cleared during the periods without fat infusion . In the group that received Pediatric Fat Emulsion 4501 the means of both free and total plasma carnitine concentrations increased significantly , whereas they tended to decrease in the Intralipid ® group Parenterally fed preterm neonates are known to be at risk for carnitine deficiency . We studied substrate utilization in low-birth-weight infants receiving total parenteral nutrition ( TPN ) with ( A ) and without ( B ) supplementation of 48 mg carnitine.kg-1.d-1 on days 4 - 7 ( birth weights 1334 + /- 282 vs 1318 + /- 248 g , gestational age 32 + /- 2 vs 32 + /- 2 wk , A vs B , respectively ) . TPN consisted of 11 g glucose.kg-1.d-1 and 2.4 g.kg-1.d-1 of both protein and fat . Plasma carnitine concentrations at day 7 were for free carnitine 11.8 + /- 5.0 vs 164 + /- 56 mumol/L and for acyl carnitine 3.8 + /- 2.0 vs 33.9 + /- 15.4 mumol/L , respectively . Indirect calorimetry at day 7 showed a higher fat oxidation ( 0.21 , -0.31 to + 0.60 vs 1.18 , 0.70 to 1.95 g. kg-1.d-1 , respectively , P less than 0.02 , median and interquartile range ) in group B and a higher protein oxidation ( 0.37 , 0.30 - 0.43 vs 0.63 , 0.53 - 0.88 g.kg-1.d-1 , P less than 0.001 ) . The time to regain birth weight was also higher in group B ( 7 , 5.5 - 9 vs 9 , 7 - 14 d , P less than 0.05 ) . Carnitine supplementation and calorie intake were the best explanatory variables for metabolic rate ( R2 = 0.45 , P less than 0.002 ) . We conclude that carnitine supplementation of TPN in this dosage does not seem advisable OBJECTIVE Carnitine is thought to be a conditionally essential biological cofactor for premature infants . A preliminary study suggested that carnitine could significantly reduce  apnea of prematurity .  The objective of this study was to evaluate critically the role of carnitine in idiopathic apnea of prematurity and to determine whether the use of carnitine would facilitate discontinuation of mechanical ventilatory support , shorten the duration of ventilatory support , and reduce the amount of time that such infants are exposed to both mechanical ventilation and oxygen . We also wanted to determine the effects of supplemental carnitine on weight gain , time to regain birth weight , time to achieve full enteral feedings , and length of hospital stay . METHODS A prospect i ve , r and omized , blinded trial was conducted on 44 preterm infants who were from the same neonatal intensive care unit and who were < or = 32 weeks ' gestational age with a postnatal age < 48 hours and a birth weight < 1500 g and required total parenteral nutrition ( TPN ) . Infants were r and omized to receive carnitine supplementation or placebo without crossover . Carnitine-supplemented infants received 30 mg/kg/d carnitine in their TPN until the they were tolerating 120 mL/kg/d enteral feedings , and then they received 30 mg/kg/d oral carnitine . The placebo group received TPN without supplemental carnitine ; when they tolerated 120 mL/kg/d enteral feedings , they received an oral placebo . The 2 groups continued on their respective supplemental carnitine or placebo until 34 weeks ' adjusted age , at which time the study period was completed . Twelve-hour cardiorespiratorygrams to record heart rate , respiratory impedance , and oxygen saturation , and a nasal thermistor to detect expiratory airflow were performed every 4 days on 3 occasions and at 30 and 34 weeks ' adjusted age . Plasma carnitine levels were measured at day 14 . RESULTS There were no significant differences between the 2 groups in the occurrence of apnea as detected by cardiorespiratorygram or nursing observation . There were no significant differences between the groups in regard to total days on ventilator , days of nasal continuous positive airway pressure , time to regain birth weight , time to reach enteral feedings of 120 mL/kg/d , discharge weight , adjusted age at discharge , need for oxygen at 28 days ' and 36 weeks ' adjusted age , or length of stay . The plasma carnitine level was a median of 15.5 micromol/L ( range : 7.6 - 30.5 ) for the placebo infants compared with a median of 195.3 micromol/L ( range : 71.7 - 343.6 ) for the carnitine infants . CONCLUSIONS In this blinded , r and omized , placebo-controlled study , we found that infants who received supplemental carnitine did not demonstrate any reduction in apnea of prematurity , ventilator or nasal continuous positive airway pressure days , or the need for supplemental oxygen therapy . Although carnitine may be of significant nutritional benefit for very low birth weight infants , our study does not support its use to reduce apnea of prematurity or decrease dependence on mechanical ventilation OBJECTIVE Systemic carnitine deficiency may present with apnea , hypotonia , and  poor growth . Premature infants often manifest these symptoms and are at risk of developing carnitine deficiency because of immaturity of the biosynthetic pathway , lack of sufficient predelivery transplacental transport , and lack of sufficient exogenous supplementation . This study was undertaken to examine the effect of carnitine supplementation in premature infants . METHODS Eighty preterm infants < 1500 g were enrolled in a prospect i ve , double-blind , placebo-controlled study of carnitine supplementation within 96 hours of delivery . Growth , length of hospital stay , and frequency and severity of apnea were the primary outcome measures . RESULTS Weight gain and change in length , fronto-occipital head circumference , mid arm circumference , and triceps skinfold thickness were similar between the carnitine-supplemented and placebo groups . The amount and severity of apnea and the overall length of hospitalization were also similar between the 2 groups . The carnitine levels in the supplemented group were significantly higher than in the placebo group at 4 and 8 weeks after study entry . CONCLUSION Although preterm infants < 1500 g have low carnitine levels , routine supplementation with carnitine has no demonstrable effect on growth , apnea , or length of hospitalization and thus seems to be unnecessary Summary The effect of a lipid emulsion containing longchain triglycerides ( LCT ) and supplemented with L-carnitine on plasma lipids and bilirubin in premature neonates on total parenteral nutrition was compared to that of lipid emulsions containing either LCT or a mixture of LCT and medium-chain triglycerides ( MCT ) . In a double-blind r and omized study 49 premature neonates received one of the three fat emulsions , given intravenously , over 16–20 h daily for 6 days . Plasma carnitine levels increased significantly in the supplemented group only ; the addition of carnitine did not seem to affect any of the parameters studied . Mean plasma triglycerides rose by 193 and 199 % in the carnitine-supplemented and the LCT groups , respectively , and by 314 % in the MCT/LCT group . On the sixth day of the study free fatty acids were significantly higher in the MCT/LCT group than in the other two groups . Plasma phospholipids and free cholesterol increased ( p < 0.05 ) progressively in all groups and were correlated ( r = 0.74 , p < 0.001 ) . At the end of the 6-day study all groups showed a similar decline in free and total bilirubin levels despite the significant increase in plasma lipids and free fatty acids result ing from the stepwise increase in lipid load . No correlation was found between free fatty acids and free bilirubin . Since hyperbilirubinemia and hypertriglyceridemia appear to be clinical ly independent factors , the infusion of lipids should not be withheld from jaundiced infants on total parenteral nutrition BACKGROUND AND AIMS Advanced glycation end products ( AGEs ) contribute to cardiovascular disease in patients with hemodialysis ( HD ) . We have recently found that carnitine levels are inversely associated with skin AGE levels in HD patients . We examined whether L-carnitine supplementation reduced skin AGE levels in HD patients with carnitine deficiency . METHODS This was a single-center study . One hundred and two HD patients ( total carnitine levels < 50 μmol/L ) were enrolled and r and omized to either oral administration of L-carnitine ( 900 mg/day ) ( n=51 ) or control ( n=51 ) . After 6 months , metabolic and inflammatory variables , including serum levels of carnitine , were measured . Skin AGE levels were determined by evaluating skin auto-fluorescence with an AGE-reader . RESULTS There were no significant differences of clinical variables at baseline between the  control and L-carnitine therapy group . Thirty-two patients did not complete the assessment or treatment of the study .  Oral L-carnitine supplementation for 6 months significantly increased low-density lipoprotein cholesterol ( LDL-C ) , triglycerides , total , free , and acyl carnitine levels , while it decreased alanine transaminase , acyl/free carnitine ratio , β₂-microglobulin , and skin AGE values . Change in total carnitine values from baseline ( Δtotal carnitine ) and Δfree carnitine were inversely associated with Δskin AGE levels  in L-carnitine-treated patients ( p=0.036 and p=0.016 , respectively ) . In multiple regression analysis , Δfree carnitine was a sole independent determinant of Δskin AGEs ( R²=0.178 ) . CONCLUSIONS The present study demonstrated that oral L-carnitine supplementation significantly decreased skin AGE levels in HD patients with carnitine deficiency . These observations suggest that supplementation of L-carnitine might be a novel therapeutic strategy for preventing the accumulation of tissue AGEs in carnitine-deficient patients with HD OBJECTIVES . Arachidonic acid ( 20:4n-6 ) and docosahexaenoic acid ( 22:6n-3 ) are essential for brain growth and cognitive development . We have reported that supplementing pregnant and lactating women with n-3 very-long-chain polyunsaturated fatty acids promotes higher IQ scores at 4 years of age as compared with maternal supplementation with n-6 polyunsaturated fatty acids . In our present study , the children were examined at 7 years of age with the same cognitive tests as at 4 years of age . We also examined the relation between plasma fatty acid pattern and BMI in children , because an association between arachidonic acid and adipose tissue size has been suggested . METHODS . The study was r and omized and double-blinded . The mothers took 10 mL of cod liver oil or corn oil from week 18 of pregnancy until 3 months after delivery . Their children were tested with the Kaufman Assessment Battery for Children at 7 years of age , and their height and weight were measured . RESULTS . We did not find any significant differences in scores on the Kaufman Assessment Battery for Children test at 7 years of age between children whose mothers had taken cod liver oil ( n = 82 ) or corn oil ( n = 61 ) . We observed , however , that maternal plasma phospholipid concentrations of α-linolenic acid ( 18:3n-3 ) and docosahexaenoic acid during pregnancy were correlated to sequential processing at 7 years of age . We observed no correlation between fatty acid status at birth or during the first 3 months of life and BMI at 7 years of age . CONCLUSION . This study suggests that maternal concentration of n-3 very-long-chain polyunsaturated fatty acids during pregnancy might be of importance for later cognitive function , such as sequential processing , although we observed no significant effect of n-3 fatty acid intervention on global IQs . Neonatal fatty acid status had no influence on BMI at 7 years of age OBJECTIVE 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 DESIGN The study was a double-blind parallel placebo-controlled  r and omized 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 256/7 and 26 to 286/7 weeks ) , and r and omized to receive , either L-carnitine at a dose of 50 μmol/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 . RESULTS Among the 63 infants enrolled in the trial , 32 were r and omized 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 . CONCLUSION Prolonged supplementation of L-carnitine did not improve long-term weight gain in very preterm infants BACKGROUND & AIMS Carnitine may be considered conditionally essential in the neonatal population . The purpose of this study was to evaluate the effects of long-term carnitine supplementation on total carnitine status and morbidity in premature neonates . METHODS In this prospect i ve , r and omized , placebo-controlled , double-blinded study , premature neonates received carnitine supplementation ( 20mg/kg/day ) or placebo .  Plasma ( nmol/ml ) and red blood cell ( RBC ) ( nmol/mg hemoglobin ) total carnitine concentrations , 24-h nitrogen excretion , intake and weight , and respiratory , gastroesophageal , and infectious morbidity were assessed . RESULTS Twenty-nine neonates ( 13 placebo , 16 carnitine ; 27+/-2 weeks gestation ; 976+/-259 g birthweight ) were studied for up to 8 weeks . Plasma total carnitine concentrations exceeded the reference range in the carnitine group ( weeks 1 - 8 ) ; however , concentrations did not reach reference range until week 4 in the placebo group . RBC total carnitine concentrations increased , but remained below reference range in both the carnitine ( weeks 1 - 6 ) and placebo ( weeks 1 - 8 ) groups . Carnitine group neonates regained their birthweight more rapidly than placebo group neonates ( day of life 11.8+/-6 vs. 16.9+/-6.3 , P=0.034 ) . In addition , percent periodic breathing calculated from cardiopulmonary trend monitor data ( weeks 1 - 8 ) was lower in the carnitine group ( 0.4+/-0.9 vs. 1.4+/-1.9 , P=0.014 ) . There was no difference with respect to other markers of respiratory , gastroesophageal and infectious morbidity or nitrogen balance . CONCLUSIONS Carnitine supplementation at 20mg/kg/day results in increased plasma and RBC total carnitine concentrations , has a positive effect on catch-up growth , and may improve periodic breathing in premature neonates Objective : The primary aim of this study was to determine if an association exists between amino-acid levels and development of cholestasis . The secondary aim of our amino-acid dose comparison trial was to identify factors associated with the development of prolonged cholestatic jaundice . Study Design : We compared demographic characteristics and amino-acid levels in neonates who developed cholestasis with those who did not . Parenteral-associated cholestatic liver disease was defined as a direct serum bilirubin above 5 mg per 100 ml any time during the first 28 days after birth in neonates with no history of biliary atresia or viral hepatitis . We obtained filter paper blood spots for amino acid and acylcarnitine measurements on the day of r and omization and days 7 and 28 of age to identify a profile of values that could be used to identify neonates with evidence of abnormal liver function . Result : We enrolled 122 neonates in our study ; 13 ( 10.7 % ) developed cholestasis . Neonates who developed cholestasis were more immature , had lower birth weight , were exposed to parenteral nutrition for a longer period , had a higher cumulative dose of amino acids , were less often on enteral nutrition by day 7 of age , more often had a patent ductus arteriosus and severe intraventricular hemorrhage and were more commonly treated with steroids by 28 days of age . Amino acid and acylcarnitine values were not different for the two groups on the day of r and omization . On day 7 ( parenteral phase of nutrition ) , blood urea nitrogen , citrulline , histidine , methionine and succinyl carnitine were higher , and serine , glutamate and thyroxine levels were lower in the neonates who developed cholestasis than in who did not . Conclusion : Cholestasis remains an important complication of parenteral nutrition , and several clinical and biochemical factors may be helpful in identifying high-risk patients AIMS Carnitine is involved in fatty acid metabolism and it is cleared by dialysis . As it plays a role in energy utilization and because malnutrition is a frequent complication of HD treatment , we studied the effects of carnitine supplementation on several nutritional parameters in HD patients . MATERIAL AND METHODS The main selection criterion was a body mass index ( BMI ; body weight/(height)2 ) < 22 kg/m2 . Fifty-three patients were enrolled to participate in this open and r and omized study . For 6 months , 28 patients received 15 mg/kg of intravenous L-carnitine at the end of each  hemodialysis ( HD ) treatment  ( Group A ) , the remaining 25 patients were controls ( Group B ) . The measured parameters were the post-dialysis body weight , serum albumin concentration ( nephelemetry ) , food intake assessed by a 3-day food question naire , nPNA ( normalized protein equivalent of nitrogen appearance ) , creatinine generation , and anthropometry . RESULTS Forty-five patients completed the study ( Group A : 14 F/9 M , 66.7 years old ; Group B : 11 F/11 M , 65.2 years old ) . At the beginning of the study , there were no differences between the groups for age , gender , HD duration , BMI , diabetes prevalence , plasma carnitine levels and measured nutritional parameters . 65.2 % and 77.3 % in each group were carnitine-deficient ( plasma total carnitine level < 35 micromol/l ) . After 6 months of L-carnitine supplementation , none of the nutritional parameters had changed in either group , except that serum albumin concentration decreased in both groups . Dividing each group according to their respective median serum albumin concentrations , daily energy and protein intakes , creatinine generation or triceps skinfold thickness did not show any difference in the various nutritional parameters with or without carnitine supplementation . CONCLUSION Carnitine supplementation , despite normalization of plasma carnitine levels , has no effect on the nutritional status of HD patients Because carnitine has been shown to decrease oxidative stress and improve endothelial cell functioning , we examined the effects of carnitine supplementation on postpr and ial flow-mediated dilation ( FMD ) and circulating biomarkers of inflammation and oxidative stress after a high-fat meal . A r and omized , double-blind , placebo-controlled , crossover study design was used . Thirty men and women ( age 30 + /- 8 year , body mass 72.9 + /- 17.1 kg , body fat 13.0 + /- 6.4 % ) participated in 2 vascular testing days , each preceded by 3 weeks of supplementation with either 2 g/day of L-Carnitine ( L-Carnitine L-Tartrate ) or placebo with a 3- to 5-week washout period between trials . Brachial artery FMD in response to 5 minutes of upper arm occlusion and circulating markers of oxidative stress and inflammation were measured in the fasting state and after a st and ardized high-fat meal . After 3 weeks of supplementation , peak FMD in the fasting state was similar between the carnitine and placebo trials , averaging 6.6 % . Peak FMD during the postpr and ial period decreased to 5.8 % at 1.5 hours during placebo and increased to 7.7 % during the carnitine trial ( n = 30 : p = 0.043 for supplement by time interaction effect ) . This improvement in postpr and ial vascular function was most dramatic in subjects who showed a decrease in peak FMD in response to the meal ( n = 15 : p = 0.003 for supplement by time interaction effect ) . There was a significant increase in postpr and ial lipemia and plasma interleukin-6 but no effect of supplementation . There were no significant postpr and ial changes or supplement effects for plasma tumor necrosis factor-alpha and malondialdehyde . In conclusion , consistent with other work showing a beneficial effect of carnitine on vascular function , these findings indicate that carnitine supplementation in healthy individuals improves postpr and ial FMD after a high-fat meal OBJECTIVES : Nonalcoholic steatohepatitis ( NASH ) is a known metabolic disorder of the liver . No treatment has been conclusively shown to improve NASH or prevent disease progression . The function of L-carnitine to modulate lipid profile , glucose metabolism , oxidative stress , and inflammatory responses has been shown . The aim of this study was to evaluate the effects of L-carnitine 's supplementation on regression of NASH . METHODS : In patients with NASH and control subjects , we r and omly dispensed one 1-g L-carnitine tablet after breakfast plus diet and one 1 g tablet after dinner plus diet for 24 weeks or diet alone at the same dosage and regimen . We evaluated liver enzymes , lipid profile , fasting plasma glucose , C-reactive protein ( CRP ) , tumor necrosis factor (TNF)-α , homeostasis model assessment (HOMA)-IR , body mass index , and histological scores . RESULTS : At the end of the study , L-carnitine-treated patients showed significant improvements in the following parameters : aspartate aminotransferase ( P=0.000 ) , alanine aminotransferase ( ALT ) ( P=0.000 ) , γ-glutamyl-transpeptidase ( γ-GT ) ( P=0.000 ) , total cholesterol ( P=0.000 ) , low-density lipoprotein ( LDL ) ( P=0.000 ) , high-density lipoprotein ( HDL ) ( P=0.000 ) , triglycerides ( P=0.000 ) , glucose ( P=0.000 ) , HOMA-IR ( P=0.000 ) , CRP ( P=0.000 ) , TNF-α ( P=0.000 ) , and histological scores ( P=0.000 ) . CONCLUSIONS : L-carnitine supplementation to diet is useful for reducing TNF-α and CRP , and for improving liver function , glucose plasma level , lipid profile , HOMA-IR , and histological manifestations of NASH The aim of the present study was to investigate the efficacy of L-carnitine therapy on the occurrence and prognosis of respiratory distress syndrome ( RDS ) . A single blind , r and omized controlled trial study was conducted on 130 infants with gestational ages of 28 - 36 weeks . Infants were assigned to experimental groups ( groups 1 and 2 ) and control groups ( groups 3 and 4 ) . Groups 1 and 3 consisted of infants with RDS , and groups 2 and 4 groups were composed of infants without RDS . The experimental groups were treated with carnitine . No statistically significant differences in serum carnitine levels were detected between the study and the control groups on day 1 of treatment ( P=0.06 ) . However , on day 7 of treatment , serum carnitine levels in the experimental groups were significantly increased ( P=0.02 ) , as compared with the control groups . The surfactant requirement value , which is how many rounds of surfactant therapy were required , was 1.56±0.97 in group 1 , and 2.12±0.99 in group 3 ( P<0.001 ) . The mean duration of mechanical ventilation required was 3.04±3.60 days in group 1 , and 4.73±5.63 days in group 3 ( P<0.001 ) . The present results indicate that carnitine supplementation in premature infants with RDS may help to increase carnitine levels , thus decreasing the duration of mechanical ventilation and surfactant requirement Summary .Long-chain polyunsaturated fatty acids ( LCP ) are considered conditionally essential nutrients for the infant born prematurely , and attempts are being made to match fatty acid profiles of formula and breast fed infants . In this double-blind , r and omized study we investigated the effects of a formula enriched with both n-6 and n-3 LCP on plasma fatty acid profiles , antioxidant status and growth of premature infants . 29 infants received either a formula devoid of LCP or a LCP supplemented formula ( 0.5 g/100 g fat linoleic acid metabolites , 0.8 g/100 g fat α-linolenic acid metabolites ) . 17 breast fed infants served as a control group . At study entry as well as two and four weeks later , plasma and urine sample s were collected , growth data obtained and food tolerance was documented . At the end of the four week study period , plasma docosahexaenoic acid ( DHA ) levels of supplemented infants were significantly higher than those of unsupplemented infants and similar to those of infants fed human milk . Plasma n-6 LCP concentrations including arachidonic acid ( AA ) were similar between groups . The plasma α-tocopherol levels of breast fed and supplemented infants were similar and tended to be lower than in infants fed the formula devoid of LCP . Urinary malondialdehyde ( MDA ) excretion of formula fed infants was significantly higher compared to infants fed human milk , but did not differ between the two formula groups . Parameters of growth and milk tolerance did not differ between groups . Our results demonstrate that plasma LCP levels similar to those of breast fed infants can be achieved with the LCP supplemented formula used in this trial , without evidence of adverse effects of the LCP enrichment
Among infants supplemented with carnitine , there was no evidence of effect on weight gain , lipid utilization or ketogenesis .
REVIEW ER 'S CONCLUSIONS We found no evidence to support the routine supplementation of parenterally fed neonates with carnitine
BACKGROUND Carnitine , a quaternary amino acid , plays an important role in the oxidation of long chain fatty acids .
Both breast milk and infant formulas contain carnitine .
However , it is not routinely provided in parenteral nutrition solutions .
Non supplemented parenterally fed infants have very low tissue carnitine levels .
The clinical significance of this is uncertain .
Carnitine deficiency may be an etiological factor in the limited ability of premature babies to utilize parenteral lipid .
In vitro studies have suggested that fatty acid oxidation is impaired when the tissue carnitine levels fall below 10 % of normal .
Therefore relative carnitine deficiency may impair fatty acid oxidation , thus reducing the available energy and impairing growth .
OBJECTIVES The primary aim of this review is to determine whether carnitine supplementation of parenterally fed neonates will improve weight gain .
The secondary aims are to determine the effect on lipid tolerance and ketogenesis .