Long‐chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase‐I activity

.  Reuter SE, Evans AM (School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA, Australia; Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia). Long‐chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Pot...

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Published inJournal of internal medicine Vol. 270; no. 1; pp. 76 - 84
Main Authors Reuter, S. E., Evans, A. M.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.07.2011
Blackwell
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Online AccessGet full text
ISSN0954-6820
1365-2796
1365-2796
DOI10.1111/j.1365-2796.2010.02341.x

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Abstract .  Reuter SE, Evans AM (School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA, Australia; Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia). Long‐chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase‐I activity. J Intern Med 2011; 270: 76–84. Objective.  The underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine’s critical role in mitochondrial energy production, it has been suggested that chronic fatigue syndrome may be associated with altered carnitine homeostasis. This study was conducted to comparatively examine full endogenous carnitine profiles in patients with chronic fatigue syndrome and healthy controls. Design.  A cross‐sectional, observational study. Setting and subjects.  Forty‐four patients with chronic fatigue syndrome and 49 age‐ and gender‐matched healthy controls were recruited from the community and studied at the School of Pharmacy & Medical Sciences, University of South Australia. Main outcome measures.  All participants completed a fatigue severity scale questionnaire and had a single fasting blood sample collected which was analysed for l‐carnitine and 35 individual acylcarnitine concentrations in plasma by LC‐MS/MS. Results.  Patients with chronic fatigue syndrome exhibited significantly altered concentrations of C8:1, C12DC, C14, C16:1, C18, C18:1, C18:2 and C18:1‐OH acylcarnitines; of particular note, oleyl‐l‐carnitine (C18:1) and linoleyl‐l‐carnitine (C18:2) were, on average, 30–40% lower in patients than controls (P < 0.0001). Significant correlations between acylcarnitine concentrations and clinical symptomology were also demonstrated. Conclusions.  It is proposed that this disturbance in carnitine homeostasis is reflective of a reduction in carnitine palmitoyltransferase‐I (CPT‐I) activity, possibly a result of the accumulation of omega‐6 fatty acids previously observed in this patient population. It is hypothesized that the administration of omega‐3 fatty acids in combination with l‐carnitine would increase CPT‐I activity and improve chronic fatigue syndrome symptomology.
AbstractList .  Reuter SE, Evans AM (School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA, Australia; Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia). Long‐chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase‐I activity. J Intern Med 2011; 270: 76–84. Objective.  The underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine’s critical role in mitochondrial energy production, it has been suggested that chronic fatigue syndrome may be associated with altered carnitine homeostasis. This study was conducted to comparatively examine full endogenous carnitine profiles in patients with chronic fatigue syndrome and healthy controls. Design.  A cross‐sectional, observational study. Setting and subjects.  Forty‐four patients with chronic fatigue syndrome and 49 age‐ and gender‐matched healthy controls were recruited from the community and studied at the School of Pharmacy & Medical Sciences, University of South Australia. Main outcome measures.  All participants completed a fatigue severity scale questionnaire and had a single fasting blood sample collected which was analysed for l‐carnitine and 35 individual acylcarnitine concentrations in plasma by LC‐MS/MS. Results.  Patients with chronic fatigue syndrome exhibited significantly altered concentrations of C8:1, C12DC, C14, C16:1, C18, C18:1, C18:2 and C18:1‐OH acylcarnitines; of particular note, oleyl‐l‐carnitine (C18:1) and linoleyl‐l‐carnitine (C18:2) were, on average, 30–40% lower in patients than controls (P < 0.0001). Significant correlations between acylcarnitine concentrations and clinical symptomology were also demonstrated. Conclusions.  It is proposed that this disturbance in carnitine homeostasis is reflective of a reduction in carnitine palmitoyltransferase‐I (CPT‐I) activity, possibly a result of the accumulation of omega‐6 fatty acids previously observed in this patient population. It is hypothesized that the administration of omega‐3 fatty acids in combination with l‐carnitine would increase CPT‐I activity and improve chronic fatigue syndrome symptomology.
The underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine's critical role in mitochondrial energy production, it has been suggested that chronic fatigue syndrome may be associated with altered carnitine homeostasis. This study was conducted to comparatively examine full endogenous carnitine profiles in patients with chronic fatigue syndrome and healthy controls.OBJECTIVEThe underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine's critical role in mitochondrial energy production, it has been suggested that chronic fatigue syndrome may be associated with altered carnitine homeostasis. This study was conducted to comparatively examine full endogenous carnitine profiles in patients with chronic fatigue syndrome and healthy controls.A cross-sectional, observational study.DESIGNA cross-sectional, observational study.Forty-four patients with chronic fatigue syndrome and 49 age- and gender-matched healthy controls were recruited from the community and studied at the School of Pharmacy & Medical Sciences, University of South Australia.SETTING AND SUBJECTSForty-four patients with chronic fatigue syndrome and 49 age- and gender-matched healthy controls were recruited from the community and studied at the School of Pharmacy & Medical Sciences, University of South Australia.All participants completed a fatigue severity scale questionnaire and had a single fasting blood sample collected which was analysed for l-carnitine and 35 individual acylcarnitine concentrations in plasma by LC-MS/MS.MAIN OUTCOME MEASURESAll participants completed a fatigue severity scale questionnaire and had a single fasting blood sample collected which was analysed for l-carnitine and 35 individual acylcarnitine concentrations in plasma by LC-MS/MS.Patients with chronic fatigue syndrome exhibited significantly altered concentrations of C8:1, C12DC, C14, C16:1, C18, C18:1, C18:2 and C18:1-OH acylcarnitines; of particular note, oleyl-L-carnitine (C18:1) and linoleyl-L-carnitine (C18:2) were, on average, 30-40% lower in patients than controls (P < 0.0001). Significant correlations between acylcarnitine concentrations and clinical symptomology were also demonstrated.RESULTSPatients with chronic fatigue syndrome exhibited significantly altered concentrations of C8:1, C12DC, C14, C16:1, C18, C18:1, C18:2 and C18:1-OH acylcarnitines; of particular note, oleyl-L-carnitine (C18:1) and linoleyl-L-carnitine (C18:2) were, on average, 30-40% lower in patients than controls (P < 0.0001). Significant correlations between acylcarnitine concentrations and clinical symptomology were also demonstrated.It is proposed that this disturbance in carnitine homeostasis is reflective of a reduction in carnitine palmitoyltransferase-I (CPT-I) activity, possibly a result of the accumulation of omega-6 fatty acids previously observed in this patient population. It is hypothesized that the administration of omega-3 fatty acids in combination with l-carnitine would increase CPT-I activity and improve chronic fatigue syndrome symptomology.CONCLUSIONSIt is proposed that this disturbance in carnitine homeostasis is reflective of a reduction in carnitine palmitoyltransferase-I (CPT-I) activity, possibly a result of the accumulation of omega-6 fatty acids previously observed in this patient population. It is hypothesized that the administration of omega-3 fatty acids in combination with l-carnitine would increase CPT-I activity and improve chronic fatigue syndrome symptomology.
The underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine's critical role in mitochondrial energy production, it has been suggested that chronic fatigue syndrome may be associated with altered carnitine homeostasis. This study was conducted to comparatively examine full endogenous carnitine profiles in patients with chronic fatigue syndrome and healthy controls. A cross-sectional, observational study. Forty-four patients with chronic fatigue syndrome and 49 age- and gender-matched healthy controls were recruited from the community and studied at the School of Pharmacy & Medical Sciences, University of South Australia. All participants completed a fatigue severity scale questionnaire and had a single fasting blood sample collected which was analysed for l-carnitine and 35 individual acylcarnitine concentrations in plasma by LC-MS/MS. Patients with chronic fatigue syndrome exhibited significantly altered concentrations of C8:1, C12DC, C14, C16:1, C18, C18:1, C18:2 and C18:1-OH acylcarnitines; of particular note, oleyl-L-carnitine (C18:1) and linoleyl-L-carnitine (C18:2) were, on average, 30-40% lower in patients than controls (P < 0.0001). Significant correlations between acylcarnitine concentrations and clinical symptomology were also demonstrated. It is proposed that this disturbance in carnitine homeostasis is reflective of a reduction in carnitine palmitoyltransferase-I (CPT-I) activity, possibly a result of the accumulation of omega-6 fatty acids previously observed in this patient population. It is hypothesized that the administration of omega-3 fatty acids in combination with l-carnitine would increase CPT-I activity and improve chronic fatigue syndrome symptomology.
Author Reuter, S. E.
Evans, A. M.
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Issue 1
Keywords Human
Acyltransferases
Enzyme
Transferases
Long chain
Deficiency
acylcarnitine
fatty acid
Lipids
Patient
Fatty acids
Carnitine O-palmitoyltransferase
Biological activity
Chronic fatigue syndrome
Medicine
carnitine palmitoyltransferase
carnitine
Language English
License CC BY 4.0
2011 The Association for the Publication of the Journal of Internal Medicine.
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Snippet .  Reuter SE, Evans AM (School of Pharmacy & Medical Sciences, University of South Australia, Adelaide, SA, Australia; Sansom Institute for Health Research,...
The underlying aetiology of chronic fatigue syndrome is currently unknown; however, in the light of carnitine's critical role in mitochondrial energy...
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SubjectTerms acylcarnitine
Adult
Aged
Biological and medical sciences
carnitine
Carnitine - analogs & derivatives
Carnitine - blood
Carnitine - deficiency
Carnitine - physiology
Carnitine O-Palmitoyltransferase - blood
carnitine palmitoyltransferase
chronic fatigue syndrome
Epidemiologic Methods
Fatigue Syndrome, Chronic - blood
Fatigue Syndrome, Chronic - enzymology
fatty acid
Female
General aspects
Humans
Male
Medical sciences
Middle Aged
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Title Long‐chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase‐I activity
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