Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The definition of dual tryptophan pathways has increased the understanding of the mind-body, body-mind dichotomy. The serotonergic pathway highlights the primary (endogenous) psychiatric disorders. The up-regulation of the kynurenine pathway by physical illnesses can cause neuropathic and immunological disorders1 associated with secondary neuropsychiatric symptoms. Tryptophan and nicotinamide deficiencies fall within the protein energy malnutrition (PEM) spectrum. They can arise if the kynurenine pathway is stressed by primary or secondary inflammatory conditions and the consequent imbalance of available catabolic/anabolic substrates may adversely influence convalescent phase efficiency. The replacement of depleted or reduced NAD+ levels and other cofactors can perhaps improve the clinical management of these disorders. Chronic fatigue syndrome (CFS) and fibromyalgia (FM) appear to meet the criteria of a tryptophan-kynurenine pathway disorder with potential neuroimmunological sequelae. Aspects of some of the putative precipitating factors have been previously outlined.2,3 An analysis of the areas of metabolic dysfunction will focus on future directions for research and management.
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PMID:Kynurenine Pathway Pathologies: do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). 2392 1

A metabolomics approach was used to explore the effects of Panax quinquefolius (PQ) and Acorus gramineus (AG) on learning and memory in rats with diabetic-induced cognitive impairment. Thirty Wistar rats were divided into three groups, namely the normal-group, model-group, and Panax quinquefolius-Acorus gramineus-group (PQ-AG-group, 1.80g/kg/d). Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65mg/kg). Cerebrospinal fluid (CSF) was collected via cisterna magna puncture, and the Morris water maze method was used to evaluate learning and memory in rats after 11 weeks of PQ-AG treatment. Metabolic profiling of CFS samples wasperformed by using UPLC-Q-TOF-MS. Compared to the normal-group, the escape latency of the Morris water mazewas significantly prolonged in model-group rats after 12 weeks (p<0.01). Compared with the model-group, however, the escape latency was significantly shortened in PQ-AG-group rats (p<0.05). In multivariate statistical analysis, we identified 33 potential biomarkers, and six biomarkers were alteredby PQ-AG. These biomarkers were involved in the metabolism of pyrimidine; nicotinate and nicotinamide; glycine, serine, and threonine; and ascorbate and aldarate. Taken collectively, our results indicate that PQ-AG can attenuate diabetic-induced cognitive impairment by affecting a variety of metabolic pathways. Our results provide an experimental basis for studying the mechanism of action of PQ-AG.
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PMID:Metabolomics study of cerebrospinal fluid from diabetic rats with cognitive impairment simultaneously treated with Panax quinquefolius and Acorus gramineus. 3327 56