Acylcarnitine profile in neonatal hypoxic-ischemic encephalopathy

López-Suárez, Olalla; Concheiro-Guisán, Ana; Sánchez‐Pintos, Paula; Cocho, José A.; Couce, María L.

doi:10.1097/md.0000000000015221

Cited by 23 publications

(18 citation statements)

References 41 publications

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“…The serum level of total L-carnitine was found to decrease in group I, and this was in agreement with Lopez-Suarez, et al (14) and Wilson et al (13) results, which revealed that change in acylcarnitine profile may be considered in the identification of HIE cases, and in the present study it also decreased in group II. This can be explained by the fact that both groups had hypoxia, perinatal asphyxia in group I, and postnatal minimal respiratory hypoxia in group II.…”

Section: Discussionsupporting

confidence: 93%

Comparative Study Between Serum Level of Total L-carnitine in Neonatal Hypoxic Ischemic Encephalopathy (HIE) and Transient Tachypnea of the Newborn (TTN)

et al. 2021

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Background: Neonatal hypoxic-ischemic encephalopathy (HIE) is one of the most common causes of cerebral palsy. Objectives: We aimed to compare the serum levels of total L-carnitine in newborns with HIE and transient tachypnea of newborn and to determine the correlation between associated demographic data, associated changes in laboratory findings, and outcome in cases with HIE. Methods: This comparative, prospective, and observational study was conducted at the Neonatal Intensive Care Unit (NICU) of University Children Hospital. All the cases of perinatal asphyxia and TTN admitted to the NICU during 2016 - 2018 were included. Results: It was found that the serum level of total L-carnitine decreased in both HIE (I) and TTN (II) cases, but the difference was not significant (5.51 ± 1.30 µmol/L in group I vs. 6.22 ± 2.56 µmol/l in group II). Male factor with changes in the serum sodium level (132.63 ± 9.30) and abnormal serum creatinine level (1.4 [0.7 - 15.0]) were significantly related to the outcome of HIE cases. Conclusions: The serum level of total L-carnitine declined in both HIE and TTN cases. Male factor with changes in serum sodium level and abnormal serum creatinine level were significantly related to the mortality of cases with HIE.

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Section: Discussionsupporting

confidence: 93%

Comparative Study Between Serum Level of Total L-carnitine in Neonatal Hypoxic Ischemic Encephalopathy (HIE) and Transient Tachypnea of the Newborn (TTN)

et al. 2021

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“…(Çam et al 2005 ). Moreover, hypoxic–ischemic neonates had significantly increased C4, C5, C5:1, C6, C6-OH, C8 levels and decreased long-chain acylcarnitine levels (López-Suárez et al 2019 ). Powers and colleagues (Powers et al 2019 ) also found that C5 and C5:1 levels were significantly increased in DS.…”

Section: Gene Expression Proteomic and Metabolomic Profiling Of Ds Amentioning

confidence: 99%

Meta-analysis of metabolites involved in bioenergetic pathways reveals a pseudohypoxic state in Down syndrome

Pecze

Randi

Szabó

2020

Mol Med

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Clinical observations and preclinical studies both suggest that Down syndrome (DS) may be associated with significant metabolic and bioenergetic alterations. However, the relevant scientific literature has not yet been systematically reviewed. The aim of the current study was to conduct a meta-analysis of metabolites involved in bioenergetics pathways in DS to conclusively determine the difference between DS and control subjects. We discuss these findings and their potential relevance in the context of pathogenesis and experimental therapy of DS. Articles published before July 1, 2020, were identified by using the search terms “Down syndrome” and “metabolite name” or “trisomy 21” and “metabolite name”. Moreover, DS-related metabolomics studies and bioenergetics literature were also reviewed. 41 published reports and associated databases were identified, from which the descriptive information and the relevant metabolomic parameters were extracted and analyzed. Mixed effect model revealed the following changes in DS: significantly decreased ATP, CoQ10, homocysteine, serine, arginine and tyrosine; slightly decreased ADP; significantly increased uric acid, succinate, lactate and cysteine; slightly increased phosphate, pyruvate and citrate. However, the concentrations of AMP, 2,3-diphosphoglycerate, glucose, and glutamine were comparable in the DS vs. control populations. We conclude that cells of subjects with DS are in a pseudo-hypoxic state: the cellular metabolic and bio-energetic mechanisms exhibit pathophysiological alterations that resemble the cellular responses associated with hypoxia, even though the supply of the cells with oxygen is not disrupted. This fundamental alteration may be, at least in part, responsible for a variety of functional deficits associated with DS, including reduced exercise difference, impaired neurocognitive status and neurodegeneration.

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“…In addition, carnitine supplementation has been shown to improve hypoxia-induced brain oxidative stress and cognitive impairment in adult rats, and in neonatal rats carnitine decreased induced hypoxia/ischemic brain neuronal cell death, oxidative stress and expression of HIF1α [ 172 , 173 , 174 ]. Acetylated-L-carnitine improved motor- and cognitive outcomes in experimental models of neonatal hypoxia and traumatic brain injury, and decreased levels of acyl-carnitine has been reported in infants suffering from neonatal hypoxic-ischemic encephalopathy, supporting carnitine to play a role in neuroprotection in the brain [ 175 , 176 , 177 , 178 ].…”

Section: Vitamin C Functions In the Brainmentioning

confidence: 99%

Vitamin C Deficiency in the Young Brain—Findings from Experimental Animal Models

Tveden‐Nyborg

2021

Nutrients

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Severe and long-term vitamin C deficiency can lead to fatal scurvy, which is fortunately considered rare today. However, a moderate state of vitamin C (vitC) deficiency (hypovitaminosis C)—defined as a plasma concentration below 23 μM—is estimated to affect up to 10% of the population in the Western world, albeit clinical hallmarks in addition to scurvy have not been linked to vitC deficiency. The brain maintains a high vitC content and uniquely high levels during deficiency, supporting vitC’s importance in the brain. Actions include both antioxidant and co-factor functions, rendering vitamin C deficiency likely to affect several targets in the brain, and it could be particularly significant during development where a high cellular metabolism and an immature antioxidant system might increase sensitivity. However, investigations of a non-scorbutic state of vitC deficiency and effects on the developing young brain are scarce. This narrative review provides a comprehensive overview of the complex mechanisms that regulate vitC homeostasis in vivo and in the brain in particular. Functions of vitC in the brain and the potential consequences of deficiency during brain development are highlighted, based primarily on findings from experimental animal models. Perspectives for future investigations of vitC are outlined.

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Acylcarnitine profile in neonatal hypoxic-ischemic encephalopathy

Abstract: Supplemental Digital Content is available in the text

Cited by 23 publications

References 41 publications

Comparative Study Between Serum Level of Total L-carnitine in Neonatal Hypoxic Ischemic Encephalopathy (HIE) and Transient Tachypnea of the Newborn (TTN)

Comparative Study Between Serum Level of Total L-carnitine in Neonatal Hypoxic Ischemic Encephalopathy (HIE) and Transient Tachypnea of the Newborn (TTN)

Meta-analysis of metabolites involved in bioenergetic pathways reveals a pseudohypoxic state in Down syndrome

Vitamin C Deficiency in the Young Brain—Findings from Experimental Animal Models

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