Low levels of serum acylcarnitine in chronic fatigue syndrome and chronic hepatitis type C, but not seen in other diseases.

Kuratsune, Hirohiko; Yamaguti, Kouzi; Lindh, Gudrun; Evengard, B.; Takahashi, Masaharu; Machii, Takashi; Matsumura, Kaname; J, Takaishi; Kawata, Soichiro; Långström, Bengt; Kanakura, Y; Kitani, Teruo; Watanabe, Yoji

doi:10.3892/ijmm.2.1.51

Cited by 24 publications

(34 citation statements)

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“…Oral L-carnitine was recently tested in patients with narcolepsy and shown to reduce their excessive daytime sleepiness (45). Similarly low serum acylcarnitine levels have been measured in patients with chronic fatigue syndrome (46), another condition with reported sleep problems (47), and L-carnitine administration has also shown some benefit in reducing fatigue (48). These studies support the growing evidence from mutant mice studies that altered fatty acid metabolism affects sleep signaling (49).…”

Section: Discussionmentioning

confidence: 63%

Effect of sleep deprivation on the human metabolome

Davies

Ang

Revell

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

426

371

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Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/ sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation.circadian rhythms | total sleep deprivation | melatonin | depression | biomarker C ircadian clocks control the timing of most daily biological processes, including cyclic changes in metabolism and the sleep/wake cycle (1). There is a clear link between the circadian timing system and metabolism (2-4), with disrupted circadian rhythms, sleep restriction, and sleep deprivation associated with metabolic disorders (obesity, insulin resistance, diabetes) and cardiovascular disease (5-8). The underlying mechanisms linking metabolic disease, circadian clock misalignment, and sleep restriction are the subject of current research, elucidation of which will require a global "systems" approach (9). Transcriptomic studies have shown that rhythmic gene expression may be affected by sleep restriction, sleep deprivation, and mistimed sleep (10-12), but, as yet, no studies have directly investigated the effect that sleep and sleep deprivation may have on the metabolic profile. Metabolic profiling, or "metabolomics," is the profiling of small-molecule metabolites and offers the potential to characterize specific metabolic phenotypes associated with disrupted circadian timing and sleep loss. Metabolomics has an advantage over other "omics" techniques, in that it directly samples the metabolic changes in an organism and integrates information from changes at the gene, transcript, an...

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Section: Discussionmentioning

confidence: 63%

Effect of sleep deprivation on the human metabolome

Davies

Ang

Revell

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

426

371

View full text Add to dashboard Cite

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“…Fatigue is regarded as ‘a riddle wrapped in a mystery inside an enigma’ by the majority of hepatology health professionals (Jones, 1995, p. 1606). Although no definitive confirmation had been achieved, the pioneering physiology researchers in this area have advanced a number of potential causes for liver disease‐related fatigue, such as decreased levels of corticotrophin‐releasing hormone, hypercytokinaemia, serum acylcarnitine and hyperammonaemia (Dietrich et al ., 1990; Swain & Maric, 1995, 1997; Plevris & Blair, 1997; Kuratsune et al ., 1998).…”

Section: Fatigue In Chronic Liver Diseasementioning

confidence: 99%

The experience of fatigue for people living with hepatitis C

Glacken

Coates

Kernohan

et al. 2003

Journal of Clinical Nursing

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Hepatitis C affects approximately 3% of the world population, with fatigue being acknowledged as the cardinal symptom. Despite growing recognition that hepatitis C fatigue impacts in a negative manner on quality of life, at the time of this study no empirical information existed regarding the nature of this fatigue or the way in which it affects a person's life. Such information is needed to enable nurses to engage in appropriate sensitive symptom management which is the core nursing activity with this population, as to date there is no vaccine or widely effective pharmacological therapy. The aim of the study was to ascertain the nature of hepatitis C fatigue. A qualitative approach using a grounded theory approach was employed. Theoretical sampling generated 28 participants for in-depth interview. Data analysis consisted of three coding processes, each type of coding having its own purpose and method. Ethical approval was obtained, both from the principal author's academic institution and the participating health care institution. Hepatitis C fatigue emerged as being multidimensional in nature, with both acute and chronic versions existing. The hepatology community is beginning to acknowledge the significant prevalence of hepatitis C fatigue. This study provides a valuable insight into its nature. This information can serve as resource for practitioners in their development of interventions to enable the hepatitis C virus population live with fatigue in a proactive manner.

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“…While some metabolite studies of individuals with ME/CFS have examined urine 5–10 , others have also focused on blood 6, 8–16 and found that energy, amino acid, nucleotide, nitrogen, hormone and oxidative stress metabolisms are disturbed. However, the methodology of these studies was largely hypothesis-driven and as a result targeted a limited number of metabolites, such as amino acids and carbohydrates, for example.…”

Section: Introductionmentioning

confidence: 99%

Metabolic profiling of a myalgic encephalomyelitis/chronic fatigue syndrome discovery cohort reveals disturbances in fatty acid and lipid metabolism

et al. 2017

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Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) remains a continuum spectrum disease without biomarkers or simple objective tests, and therefore relies on a diagnosis from a set of symptoms to link the assortment of brain and body disorders to ME/CFS. Although recent studies show various affected pathways, the underlying basis of ME/CFS has yet to be established. In this pilot study, we compare plasma metabolic signatures in a discovery cohort, 17 patients and 15 matched controls, and explore potential metabolic perturbations as the aftermath of the complex interactions between genes, transcripts and proteins. This approach to examine the complex array of symptoms and underlying foundation of ME/CFS revealed 74 differentially accumulating metabolites, out of 361 (P<0.05), and 35 significantly altered after statistical correction (Q<0.15). The latter list includes several essential energy-related compounds which could theoretically be linked to the general lack of energy observed in ME/CFS patients. Pathway analysis points to a few pathways with high impact and therefore potential disturbances in patients, mainly taurine metabolism and glycerophospholipid metabolism, combined with primary bile acid metabolism, as well as glyoxylate and dicarboxylate metabolism and a few other pathways, all involved broadly in fatty acid metabolism. Purines, including ADP and ATP, pyrimidines and several amino acid metabolic pathways were found to be significantly disturbed. Finally, glucose and oxaloacetate were two main metabolites affected that have a major effect on sugar and energy levels. Our work provides a prospective path for diagnosis and understanding of the underlying mechanisms of ME/CFS.

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Low levels of serum acylcarnitine in chronic fatigue syndrome and chronic hepatitis type C, but not seen in other diseases.

Cited by 24 publications

References 0 publications

Effect of sleep deprivation on the human metabolome

Effect of sleep deprivation on the human metabolome

The experience of fatigue for people living with hepatitis C

Metabolic profiling of a myalgic encephalomyelitis/chronic fatigue syndrome discovery cohort reveals disturbances in fatty acid and lipid metabolism

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