Long-chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase-I activity
Article first published online: 19 JAN 2011
© 2011 The Association for the Publication of the Journal of Internal Medicine
Journal of Internal Medicine
Volume 270, Issue 1, pages 76–84, July 2011
How to Cite
Reuter, S. E. and Evans, A. M. (2011), Long-chain acylcarnitine deficiency in patients with chronic fatigue syndrome. Potential involvement of altered carnitine palmitoyltransferase-I activity. Journal of Internal Medicine, 270: 76–84. doi: 10.1111/j.1365-2796.2010.02341.x
- Issue published online: 16 JUN 2011
- Article first published online: 19 JAN 2011
- Accepted manuscript online: 22 DEC 2010 12:40PM EST
- carnitine palmitoyltransferase;
- chronic fatigue syndrome;
- fatty acid
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.