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)

Fat oxidation is important for maintaining health and for supplying energy for exercise. We have proposed that the predisposition for individual rates of fat oxidation is determined genetically but may be modulated by acute exercise or exercise training. The purpose of this study was to examine cellular fat oxidation in white blood cells (WBC) using [9,10-3H]palmitic acid. Sedentary controls free of symptoms (SED-C, n=32), were compared with known carnitine palmitoyltransferase (CPT) II-deficient patients (n =2), patients with fatiguing diseases (chronic fatigue syndrome, CFS, n=6; multiple sclerosis, MS, n=31), obesity (OB, n=5), eating disorders (ED, n=16), sedentary individuals prior to and after exercise (SED-Ex, n=12), exercise-trained sedentary individuals (SED-Tr, n=12), and elite runners (ER, n=5). Fat oxidation in WBC for all subjects was normally distributed (mean=0.270 +/- 0.090 nmol/h per 10(9) WBC) and ranged from 0.09 nmol/h per 10(9) WBC in CPT II-deficient patients to 0.59 nmol/h per 10(9) WBC in ER. There were no significant sex or acute exercise effects on WBC fat oxidation. Patients with MS, OB or ED were not different from SED-C; however, in CPT II-deficient patients, fat oxidation was low, while that of CFS patients was high. Exercise training in SED-C resulted in a 16% increase in fat oxidation but in ER it was still 97% higher than in SED-C. We propose that while WBC fat oxidation is not significantly affected by sex or acute exercise, and only by 15-20% with training, genetic factors play a role in determining both high and low fat oxidation in certain groups of individuals. The genetic predisposition for individual rates of fat oxidation may be easily measured using WBC fat oxidation, as has been shown for CPT II-deficient patients and for elite runners. Ranges of WBC fat oxidation that are abnormally low (<20 nmol/h per 10(9) WBC, normal 20-35) or high (>35 nmol/h per 10(9) WBC) are proposed based on genetic factors evaluated in this study.
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PMID:The distribution of white blood cell fat oxidation in health and disease. 1497 Jul 49

Chronic fatigue syndrome (CFS) is a disease that can seriously impair one's quality of life; patients complain of excessive fatigue and myalgia following physical exertion. This disease may be associated with abnormalities in genes affecting exercise tolerance and physical performance. Adenosine monophosphate deaminase (AMPD1), carnitine palmitoyltransferase II (CPT2), and the muscle isoform of glycogen phosphorylase (PYGM) genes provide instructions for producing enzymes that play major roles in energy production during work. The aim of this study was to look for evidence of genotype-associated excessive muscle fatigue. Three metabolic genes (AMPD1, CPT2, and PYGM) were therefore fully sequenced in 17 Italian patients with CFS. We examined polymorphisms known to alter the function of these metabolic genes, and compared their genotypic distributions in CFS patients and 50 healthy controls using chi-square tests and odds ratios. One-way analysis of variance with F-ratio was carried out to determine the associations between genotypes and disease severity using CF scores. No major genetic variations between patients and controls were found in the three genes studied, and we did not find any association between these genes and CFS. In conclusion, variations in AMPD1, CPT2, and PGYM genes are not associated with the onset, susceptibility, or severity of CFS.
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PMID:Genetic evaluation of AMPD1, CPT2, and PGYM metabolic enzymes in patients with chronic fatigue syndrome. 2752