Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of untrained, healthy, obese women (body mass index 32.5 +/- 0.9 kg.m-2) were subjected to a protocol of intense exercise on a cycloergometer and compared with lean controls (body mass index 20. 9 +/- 0.5 kg.m-2). Physiological parameters, blood lactate, bicarbonate, plasma metabolites, oxygen consumption and CO2 production were measured. Impedance-derived extracellular water and plasma changes in lactate and bicarbonate were used to determine changes in bicarbonate pools and lactate-displaced CO2. From these and respiratory gases, the respiratory quotient was calculated and thence overall fuel consumption. Anaerobic energy during exercise accounted for about 1.8% of all energy consumed in the lean but only 0.7% in the obese. Obese women fatigued at lower workloads and energy expenditure levels than did the lean, and their lactate buildup was similar when compared on the basis of fat-free mass. The data support the postulation of fatigue being triggered by a combination of factors: stretched cardiovascular work would be the main factor for obese women, in part limiting lactate production. For lean women, the triggering factor for fatigue could be the loss of buffering capacity; but it is the combination of stretching cardiovascular capacity, exhaustion of glycogen and available glucose and increase in lactate/loss of bicarbonate buffer that determines the onset of fatigue.
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PMID:During intense exercise, obese women rely more than lean women on aerobic energy. 944 96

The prevalence of obesity in industrialized countries is increasing in spite of decreased energy and fat intakes. This trend might be mainly a consequence of a decline in energy expenditure. It is suggested here that it might also be accounted for by the increasing proportion of protein in the diet, affecting the hormonal status. The nutrient imbalance is particularly apparent in early childhood, when a low fat and high protein diet is not justified because of high energy needs for growth and because it is the period of high rate of myelinization of the nervous system. At later ages, the proportion of fat exceeds the recommended level, and the protein intake remains high. A diet containing less animal and more vegetable products would reduce both protein and saturated fat excesses and could help decrease metabolic risk factors.
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PMID:Nutrient balance and body composition. 947 39

Brown adipose tissue (BAT) has the capacity for uncoupled mitochondrial respiration and is proposed to be a key site for regulating energy expenditure in rodents. To better define the role of BAT in energy homeostasis, we previously created a line of transgenic mice with deficiency of BAT (UCP promoter-driven diphtheria toxin A transgenic mice [UCP-DTA]) mice. These mice develop obesity that initially is due to decreased energy expenditure and later accompanied by hyperphagia despite increased levels of circulating leptin. In addition, the obesity of these mice is accompanied by severe insulin-resistant diabetes and hyperlipidemia. To better define the basis for leptin resistance in this model, we treated UCP-DTA mice with leptin (300 microg i.p., b.i.d.) and compared their response with that of leptin-treated ob/ob and FVB control mice (30 microg i.p., b.i.d.). Leptin treatment of FVB and ob/ob mice decreased their body weight and food intake and improved their glucose homeostasis. In contrast, tenfold higher dosages of leptin had no effect on body weight, food intake, or circulating insulin or glucose concentrations of UCP-DTA mice. Hypothalamic neuropeptide Y (NPY) mRNA expression was lower in UCP-DTA mice than in littermate control FVB mice in the fed state, and increased progressively in response to food restriction as leptin levels fell. In parallel to the levels of hypothalamic NPY, corticosterone levels were initially suppressed and rose with food restriction. Thus food intake, body weight, and insulin and glucose homeostasis of UCP-DTA mice are all extraordinarily resistant to leptin, whereas hypothalamic NPY and the hypothalamopituitary adrenal (HPA) axis may remain under leptin control. Further elucidation of the mechanisms underlying leptin resistance in UCP-DTA mice may provide valuable insights into the basis for leptin resistance in human obesity.
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PMID:Severe leptin resistance in brown fat-deficient uncoupling protein promoter-driven diphtheria toxin A mice despite suppression of hypothalamic neuropeptide Y and circulating corticosterone concentrations. 951 18

The effects of objective and subjective overload, and of physical and emotional burnout, on cholesterol and triglycerides levels were studied in a quasiprospective design. The possible moderating effects of emotional reactivity on these relationships were also investigated. The study's hypotheses were tested separately for male and female employees. Time 1 (T1) data were collected from 665 healthy employees (30% women) while they were undergoing periodic health examinations in a health-screening center. Time 2 (T2) measures of cholesterol and triglycerides were collected 2 to 3 years after T1. The hypotheses were tested by regressing each T2 criterion on its T1 level; the control variables of age, obesity, diet, alcohol consumption, and smoking; and the other predictors. For female employees, the T2-T1 changes in the serum lipids were positively predicted by emotional burnout, as expected, but negatively predicted by physical fatigue. For male employees, both types of T1 burnout were positive predictors of the T2-T1 change in total cholesterol.
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PMID:Effects of work overload and burnout on cholesterol and triglycerides levels: the moderating effects of emotional reactivity among male and female employees. 955 97

Massive overweight is an increasing health problem and underlies several complications which in turn result in premature death. The mechanisms underlying the imbalance between energy intake and energy expenditure, that lead to obesity in humans, are still only partly understood. In rodents, heat generation and the burning of calories by the mitochondrial uncoupling protein 1 (UCP1) are important for metabolic control. However, UCP1 is exclusively expressed in brown fat which is only present in limited amounts in human adults. The recent characterization of two new uncoupling proteins, UCP2 and UCP3, may elucidate potentially important pathways for energy expenditure regulation in man. The aim of this study was to investigate whether obesity is accompanied by aberrations in UCP2 and UCP3 regulation. Expression of these two genes was examined using in situ hybridization in six lean and six obese, but otherwise healthy, men. The UCP2 expression was decreased by 28 % (p = 0.001) in the abdominal muscle of the obese subjects. No differences in UCP3 expression were observed between obese and control subjects, although there was great variation in the expression between subjects. In conclusion, these data suggest an impaired activity of the mitochondrial uncoupling protein UCP2, but probably not UCP3, in obese subjects. This may result in decreased energy expenditure and contribute to the development and maintenance of obesity.
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PMID:Reduced gene expression of UCP2 but not UCP3 in skeletal muscle of human obese subjects. 972 96

Brown adipose tissue-deficient [uncoupling protein (UCP)-promoter-driven diphtheria toxin A (DTA)] mice develop obesity as a result of both decreased energy expenditure and hyperphagia. The hyperphagia occurs despite high serum leptin levels. Hence, this is a model of leptin-resistant obesity in which the mechanism driving hyperphagia is unknown. Leptin is a regulator of a number of hypothalamic neuropeptides involved in energy homeostasis. In ob/ob mice, leptin deficiency results in increased expression of neuropeptide Y (NPY), agouti-related protein (AGRP), and melanin-concentrating hormone (MCH), and decreased expression of POMC. We have previously shown that NPY is reduced in the UCP-DTA mouse, suggesting a normal NPY response to leptin. To define other potential sites of leptin resistance, we used in situ hybridization to evaluate the expression of messenger RNAs (mRNAs) encoding a number of peptides, including NPY, AGRP, MCH, and POMC. We confirmed that the decrease in NPY expression previously detected by Northern blots reflects a decrease in NPY expression in the arcuate nucleus. AGRP mRNA was also decreased, whereas POMC mRNA levels in the arcuate nucleus were the same as control. MCH mRNA levels in the lateral hypothalamic area were also decreased. In contrast, there was induction of NPY expression in the dorsomedial hypothalamic nucleus in the UCP-DTA animals but not in the controls. The results indicate that these neuropeptides generally respond to leptin and that the hyperphagia seen in the UCP-DTA mice is likely the result of dysregulated expression of other, as yet unexamined, hypothalamic peptides, or lies at sites distal to the hypothalamus.
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PMID:Characterization of expression of hypothalamic appetite-regulating peptides in obese hyperleptinemic brown adipose tissue-deficient (uncoupling protein-promoter-driven diphtheria toxin A) mice. 979 75

To evaluate the weight reducing effect of fluoxetine on steroid-induced obesity, we conducted an open, clinical intervention study of 20-40 mg/day fluoxetine, 24 weeks duration. Thirteen myasthenia gravis, overweight, long-term steroid-treated patients [age: 31-59, body mass index (BMI): 29-54 kg/m2] were included. Measurements of weight, BMI, and routine laboratory tests, were undertaken at baseline, 12 and 24 weeks. Muscle strength and fatigue parameters were assessed at 4 week intervals. Fluoxetine induced mean weight loss of 7.7+/-2.6 kg and 10.3+/-2.9 kg over a period of 12 and 24 weeks respectively, (P<0.05). Mean BMI decreased from 35.8 to 32.2 kg/m2 over the study period. No significant side effects were noted. We conclude that patients suffering from steroid-induced obesity respond to fluoxetine treatment of overweight by significant weight loss.
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PMID:Fluoxetine treatment for weight reduction in steroid-induced obesity: a pilot study in myasthenia gravis patients. 1008 36

A retrospective analysis of Cushing's syndrome from the retrieved records of 24 out of a total of 27 referred cases over a period of 10 years (January 1985-January 1995) showed confirmation in 16 cases. Fourteen (88%) were females, 9 (56%) were in their third decade. Duration of symptoms before admission was one year or less in eleven (69%) patients. Among symptoms weakness, fatigue and weight gain and among signs moon face, truncal obesity and buffalo hump were found in all patients. Amenorrhea occurred in all the women of childbearing age. Basal urinary 17-hydroxycorticoid (17-OHCS) values were elevated in 9/12 patients and low dose dexamethasone suppression test favoured Cushing's syndrome in 8/9 patients. Definitive treatment consisted of bilateral adrenalectomy in 7 and transfrontal pituitary adenomectomy in 3. Two patients declined surgery; 4 patients were lost to follow up before definitive treatment. Two patients who had bilateral adrenalectomy and two who had transfrontal adenomectomy died subsequently while three remained in good health on corticosteroid replacement therapy. Three of the 7 patients who had bilateral adrenalectomy developed Nelson's syndrome. It is concluded that Cushing's disease is the most frequent cause of Cushing's syndrome in our series. The patients presented with the well-known clinical manifestations of hypercortisolism. However, our laboratory facilities require considerable improvement to serve as a reliable adjunct to clinical evaluation. Since Cushing's syndrome, whatever the cause, is eventually fatal if left untreated, surgical intervention is mandatory after confirmation of the cause with appropriate laboratory tests.
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PMID:Cushing's syndrome: a ten year experience at Tikur Anbassa Hospital. 1021 44

Obstructive sleep apnea hypoventilation syndrome (OSAHS) is an important public health problem. However, major gaps exist in our knowledge about the clinical features of this disorder in the pediatric age group. The purpose of this study was to examine clinical features of OSAHS diagnosed by polysomnography in otherwise healthy children. In this cross-sectional study, 326 children without underlying medical conditions (5.8+/-3.0 years, range 1-12 years; 56% male) were recruited from patients referred by primary care and otorhinolaryngology physicians for evaluation of snoring and difficulty breathing. Ethnic group distribution was African-American (38%), Caucasian (30%), and Hispanic (31%). Complaints of daytime tiredness or sleepiness were reported in 29% of the children. All children underwent overnight polysomnography (N = 330 studies). OSAHS was diagnosed in 59% of the children, based on polysomnographic criteria. The remaining children had either primary snoring (25%); no snoring (10%), or upper airway resistance syndrome (6%). Neither male gender nor obesity increased the likelihood for the diagnosis of OSAHS. However, the incidence of obesity in the study population (28%) was more than twice that of the general pediatric population. African-American children had a greater likelihood for OSAHS diagnosis compared to Hispanic or Caucasian children. Daytime complaints of sleepiness or tiredness were not more common in children diagnosed with OSAHS than in the children without OSAHS. As expected, tonsillar hypertrophy increased the likelihood of OSAHS diagnosis. In summary, many of the clinical features of childhood OSAHS are in marked contrast to those in adults.
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PMID:Clinical features of obstructive sleep apnea hypoventilation syndrome in otherwise healthy children. 1038 92

The symptomatology associated with severe growth hormone (GH) deficiency in adult life is a real entity but unfortunately it is also nonspecific with extreme fatigue and obesity dominating the clinical picture. Quality of life (QOL) is a term widely used by clinicians, research scientists and policy-makers, though there is a lack of consensus over its definition. Most of the related literature lists aspects assumed to be components of QOL and most measures are based upon the assumption that QOL is related to the ability to function in certain domains of physical, social and environmental existence such as work, leisure pursuits, socializing, etc. Most published studies on QOL have utilized generic measures of health status which were developed more than 20 years ago, were not designed for clinical trials, and it is debatable whether all the questions are relevant to patients. Only the Nottingham Health Profile has content derived entirely from lay people as opposed to being written by professionals. This has led to the development of QOL measures specific for GH deficiency based on unstructured qualitative interviews (1-2 h), which, unfortunately, have been carried out in a relatively small number of patients. Furthermore, the disease-specific measures of QOL are not truly specific for GH deficiency, as the patient has in almost all cases had a pituitary tumor, undergone surgery and/or radiotherapy and is receiving other hormone therapy for additional pituitary hormone deficits. Should the ideal control population for comparison with the GH-deficient patient cohort be normal subjects or patients with chronic disorders? Placebo-controlled studies of GH therapy indicate a definite placebo effect contributing to the improvement in QOL in GH-deficient adults. QOL is generally stated to be less affected in young adults with childhood-onset GH deficiency compared with patients with adult-onset GH deficiency. How do we know? Do we have disease-specific measures applicable to the adolescent age group? In reality, many centres utilize reduced QOL as an indication for GH replacement. However, heavy reliance is placed on the subjective patient interview rather than objective use of a disease-specific questionnaire. Why? Because there is no questionnaire score (number) available to reflect degree of impairment of QOL at baseline or of improvement in QOL in response to GH therapy.
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PMID:The use of self-rating questionnaires as a quantitative measure of quality of life in adult growth hormone deficiency. 1044 81


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