Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The involvement of glucocorticoids (GC) in the development of diet-induced obesity and in the concomitant adaptations of triglyceride (TG)-rich lipoprotein metabolism were examined. Rats were fed either rodent chow, which maintains a low lipid flux, or a diet high in sucrose and fat (HSF) that increases lipid flux, leading to metabolic perturbations similar to those that define the plurimetabolic syndrome in humans. The GC status was manipulated through adrenalectomy (ADX) and corticosterone (Cort) replacement. Compared with chow, the HSF diet increased energy intake (17%) and whole body (8%) and adipose tissue (80%) weights. The HSF diet also increased the acute postprandial rise in plasma insulin (4-fold) and TG (3-fold), fasting liver TG content (3-fold), triglyceridemia (54%), and adipose tissue lipoprotein lipase (LPL) activity (2-fold). ADX decreased energy intake and whole body and adipose tissue weights in both dietary cohorts, but more so in HSF-fed than in chow-fed animals. These ADX-induced effects were totally prevented by Cort replacement in rats fed chow, but only partially so in those fed the HSF diet in proportion to the degree of restoration of energy intake. In the chow-fed cohort, the above indexes of TG metabolism remained unaffected by the Cort status, whereas in the HSF-fed cohort, these variables were decreased by ADX to levels of chow-fed animals. Cort replacement in the HSF-fed animals restored indexes of TG metabolism to intact levels and reestablished the diet-related differences observed in intact animals. These findings indicate that GC modulate fasting TG metabolism only minimally when a diet that maintains a low lipid flux is fed. In contrast, their presence is a necessary condition for the development of diet-induced obesity and the concomitant alterations in insulin sensitivity and TG-rich lipoprotein metabolism.
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PMID:Modulation of triglyceride metabolism by glucocorticoids in diet-induced obesity. 1044 52

Dieting or a change in eating habits is the most widely used approach aimed at reducing body weight. However, it is also well known that many obese people cannot reduce body weight substantially, no matter how hard they try, and that they soon regain whatever they do lose. The conventional approach to the treatment of obesity is to control it by prohibition or suppression of overeating, and by orders to change eating habits. This paper presented and examined a new psychosomatic approach for obesity (NPAO). Taking the story of "The North Wind and the Sun" from Aesop's Fables as a metaphor, this hypothesis is based on the reduction of overstressors through a "Sun"-type approach as opposed to a "North Wind"-type approach. This "Sun"-type approach, which incorporates 2 principles and 3 basic rules, is useful in decreasing stressors such as prohibition, suppression and orders, and increasing pleasantness, which competes with unpleasant stress. The treatment based on this hypothesis was applied to 77 subjects: 62 men (age 46.2 +/- 8.0 years) and 15 women (age 50.6 +/- 4.5 years). All subjects were given medical checks just before and 6 months after the psychosomatic approach for obesity. For a proportion of cases, maximal oxygen uptake (VO2max) was measured before and after. In the practiced group (48 cases) except for three persons who had stopped the program within 3 months after the start, body weight and body mass index fell significantly by 5.2 kg (p < 0.001) and 2.0 kg/m2 (p < 0.001) respectively, after 6 months. There were significant reductions in total cholesterol and triglyceride (p < 0.01, p < 0.01 respectively). VO2max, however, increased significantly (p < 0.05). The subjects' impressions of this therapy, collected after 6 months were as follows: "It was comfortable" 67.7%, "It was hard going" 8.8%, "My body has become lighter" 79.4%, "I have become more energetic" 70.5%, and "I have become happier" 64.7%. During the period of the therapy, there was no report of any appearance of new physical or mental abnormalities such as fatigue or uncomfortableness. On the other hand, there were no significant changes in any parameters except for an increase of blood sugar in the non-practiced group (26 cases). These results strongly indicate that the NPAO is easy in practice, has a high success rate, shows no rebounding, reduces body weight safely, and results in an increase of vigor.
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PMID:Proposal of a new hypothesis for the psychosomatic treatment of obesity and its application. 1053 2

Sleep apnea and associated daytime sleepiness and fatigue are common manifestations of mainly obese middle-aged men. The onset of sleep apnea peaks in middle age, and its morbid and mortal sequelae include complications from accidents and cardiovascular events. The pathophysiology of sleep apnea remains obscure. The purpose of this study was to test three separate, albeit closely related, hypotheses. 1) Does sleep apnea contribute to the previously reported changes of plasma cytokine (tumor necrosis factor-alpha and interleukin-6) and leptin levels independently of obesity? 2) Among obese patients, is it generalized or visceral obesity that predisposes to sleep apnea? 3) Is apnea a factor independent from obesity in the development of insulin resistance? Obese middle-aged men with sleep apnea were first compared with nonapneic age- and body mass index (BMI)-matched obese and age-matched lean men. All subjects were monitored in the sleep laboratory for 4 consecutive nights. We obtained simultaneous indexes of sleep, sleep stages, and sleep apnea, including apnea/hypopnea index and percent minimum oxygen saturation. The sleep apneic men had higher plasma concentrations of the adipose tissue-derived hormone, leptin, and of the inflammatory, fatigue-causing, and insulin resistance-producing cytokines tumor necrosis factor-alpha and interleukin-6 than nonapneic obese men, who had intermediate values, or lean men, who had the lowest values. Because these findings suggested that sleep apneics might have a higher degree of insulin resistance than the BMI-matched controls, we studied groups of sleep-apneic obese and age- and BMI-matched nonapneic controls in whom we obtained computed tomographic scan measures of total, sc, and visceral abdominal fat, and additional biochemical indexes of insulin resistance, including fasting plasma glucose and insulin. The sleep apnea patients had a significantly greater amount of visceral fat compared to obese controls (<0.05) and indexes of sleep disordered breathing were positively correlated with visceral fat, but not with BMI or total or sc fat. Furthermore, the biochemical data confirmed a higher degree of insulin resistance in the group of apneics than in BMI-matched nonapneic controls. We conclude that there is a strong independent association among sleep apnea, visceral obesity, insulin resistance and hypercytokinemia, which may contribute to the pathological manifestations and somatic sequelae of this condition.
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PMID:Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia. 1072 86

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

The principal risk factors of osteoarthritis of the knee are: age, obesity and gender. It is hypothesized that long-duration walking (e. g. 20 min) in the elderly obese will lead to quadriceps fatigue. Changes in the gait pattern due to fatigue will lead to altered knee kinematics at heelstrike and consequently decreased shock absorption. This scenario will result in an increased rate of loading and possibly an increase in the overall magnitude of peak ground reaction forces, both of which could cause articular cartilage degeneration. Obese females are at an overall higher risk of developing osteoarthritis than males. This gender discrepancy may be explained by the fact that females have a higher percentage of body fat content (lower proportion of lean mass) that may increase the rate of quadriceps fatigue. These biomechanical hypotheses can be examined by studying continuous periods of walking in which ground reaction forces, knee kinematics and electromyography data are recorded.
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PMID:Obesity and osteoarthritis of the knee: hypotheses concerning the relationship between ground reaction forces and quadriceps fatigue in long-duration walking. 1079 Jul 48

Nonalcoholic steatohepatitis (NASH) is a histological diagnosis applied to a constellation of liver biopsy findings that develop in the absence of alcohol abuse. Steatosis, a mixed cellular inflammatory infiltrate across the lobule, evidence of hepatocyte injury and fibrosis are the findings that can be seen. This entity is often identified during evaluation of elevated aminotransferases after exclusion of viral, metabolic and other causes of liver disease. Obesity is a major risk factor for NASH. The role of diabetes is less certain, although evidence is accumulating that hyperinsulinism may play an important pathophysiological role. Patients sometimes suffer from right upper quadrant abdominal pain and fatigue; examination may reveal centripetal obesity and hepatomegaly. Although patients are often discovered because of persistent aminotransferase elevations, these enzymes can be normal in NASH. When they are elevated, the alanine aminotransferase level is typically significantly greater than the aspartate aminotransferase level. This can be particularly helpful for excluding occult alcohol abuse. Imaging studies identify hepatic steatosis when the amount of fat in the liver is significant; however, imaging does not distinguish benign steatosis from NASH. Ultimately a liver biopsy is needed to diagnose NASH. The biopsy may be useful for establishing prognosis based on the presence or absence of fibrosis and for excluding other unexpected causes of liver enzyme elevations. Weight loss is the mainstay of treatment for obese patients. About 15% to 40% of NASH patients develop fibrosis; how many of these cases progress to cirrhosis is unknown, but about 1% of liver transplants are performed with a pretransplant diagnosis of NASH.
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PMID:Nonalcoholic steatohepatitis: an evolving diagnosis. 1079 85

Feeding is a complex process responsive to sensory information related to sight and smell of food, previous feeding experiences, satiety signals elicited by ingestion and hormonal signals related to energy balance. Dopamine released in specific brain regions is associated with pleasurable and rewarding events and may reinforce positive aspects of feeding. Dopamine also influences initiation and coordination of motor activity and is required for sensorimotor functions. Thus, dopamine may facilitate integration of sensory cues related to hunger, initiating the search for food and its consumption. Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens, where they modulate movement and reward. There are projections from the nucleus accumbens to the lateral hypothalamus that regulate feeding. Dopamine-deficient mice (Dbh(Th/+), Th-/-; hereafter DD mice) cannot synthesize dopamine in dopaminergic neurons. They gradually become aphagic and die of starvation. Daily treatment of DD mice with L-3,4-dihydroxyphenylalanine (L-DOPA) transiently restores brain dopamine, locomotion and feeding. Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia. As the hypothalamic leptin-melanocortin pathway appears to regulate appetite and metabolism, we generated mice lacking both dopamine and leptin (DD x Lep(ob/ob)) to determine if leptin deficiency overcomes the aphagia of DD mice. DD x Lep(ob/ob) mice became obese when treated daily with L-DOPA, but when L-DOPA treatment was terminated the double mutants were capable of movement, but did not feed. Our data show that dopamine is required for feeding in leptin-null mice.
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PMID:Dopamine is required for hyperphagia in Lep(ob/ob) mice. 1080 66

The apparent obesity epidemic in the industrialized world is not explained completely by increased food intake or decreased energy expenditure. Once obesity develops in genetically predisposed individuals, their obese body weight is avidly defended against chronic caloric restriction. In animals genetically predisposed toward obesity, there are multiple abnormalities of neural function that prime them to become obese when dietary caloric density and quantity are raised. Once obesity is fully developed, these abnormalities largely disappear. This suggests that obesity might be the normal state for such individuals. Formation of new neural circuits involved in energy homeostasis might underlie the near permanence of the obese body weight. Such neural plasticity can occur during both nervous system development and in adult life. Maternal diabetes, obesity, and undernutrition have all been associated with obesity in the offspring of such mothers, especially in genetically predisposed individuals. Altered brain neural circuitry and function often accompanies such obesity. This enhanced obesity may then be passed on to subsequent generations in a feed-forward, upward spiral of increasing body weight across generations. Such findings suggest a form of "metabolic imprinting" upon genetically predisposed neural circuits involved in energy homeostasis. Centrally acting drugs used for obesity treatment lower the defended body weight and alter the function of neural pathways involved in energy homeostasis. But they generally have no permanent effect on body weight or neural function. Thus, early identification of obesity-prone mothers, infants, and adults and treatment of early obesity may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals.
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PMID:The obesity epidemic: metabolic imprinting on genetically susceptible neural circuits. 1093 11

In order to evaluate the characteristics of fatigue symptoms and their association with the life style and the health status, we examined using data accumulated by the longitudinal surveys from 1992 to 1998, in 118 six-year primary school children and 129 second-year junior high school children. The complaints of "drowsiness and dullness", such as "become drowsy" (71%), "give a yawn" (59%) and "want to lie down" (51%), respectively, were most frequently observed. The proportion of these complaints was high before the first morning class, but decreased when the children leave school. Notably, the complaints of "difficulty in concentration" annually have increased. Children with undesirable eating habits, particularly those who often eat salty foods, or poor life style, such as staying up late at night tended to have more complaints of fatigue symptoms. By correlation analysis, these complaints were significantly related to the obesity degree, blood pressure, HDL cholesterol and atherogenic index. These results support the hypothesis that fatigue symptoms increase or are associated with life style and health status. Consequently, it is necessary to improve the life style such as dietary habits and rhythm of life for the reduction of fatigue symptom.
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PMID:The characteristics of fatigue symptoms and their association with the life style and the health status in school children. 1095 6

The rapidly rising prevalence of obesity, worldwide, has prompted re-evaluations of the definitions and diagnostic criteria, and of the extent of the burden it contributes to health care services. Although categorized arbitrarily for epidemiological purposes according to BMI > 25 kg/m2 ('overweight') and BMI > 30 kg/m2 ('obese'), the disease itself (ICD code E.66) is the process of excess fat accumulation. It leads to multiple organ-specific pathological consequences, particularly if there is a tendency to intra-abdominal fat accumulation. The simplest field method to identify obesity and risk of medical problems is the waist circumference, and this method has found a special role in health promotion. Risks begin with waist > 80 cm (women) or > 94 cm (men). As a broad generalization, obesity produces few symptoms below the age of 40 years, but then several symptoms often develop; tiredness, breathlessness, back pain, arthritis, sweatiness, poor sleeping, depression and menstrual disorders all being common. The symptoms are often attributed to diseases in other body systems. Metabolic diseases like diabetes, hyperlipidaemia and, hypertension develop later, but the mean BMI at diagnosis of diabetes is 28 kg/m2. Ultimately, obesity increases the likelihood of myocardial infarction, stroke and several major cancers, but its biggest impact on health, especially in the elderly, is probably the multiplicity of effects on other body systems. The greatest challenge for public health is to develop effective preventive measures, recognizing that BMI > 25 kg/m2 before the age of 20 years is a very strong predictor of obesity and ill health in adulthood.
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PMID:Pathophysiology of obesity. 1099 48


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