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 in | Journal of internal medicine Vol. 270; no. 1; pp. 76 - 84 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.07.2011
Blackwell |
Subjects | |
Online Access | Get full text |
ISSN | 0954-6820 1365-2796 1365-2796 |
DOI | 10.1111/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. |
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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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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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