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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is an obesity epidemic in the industrialized world that is not simply explained by excess energy intake and decreased energy expenditure. Persistent obesity develops when genetically predisposed individuals are in a chronic state of positive energy balance. Once established, the obese body weight is avidly defended against both over- and underfeeding. Animal studies have shown that lean individuals who are genetically predisposed toward obesity have abnormalities of neural function that prime them to become obese when caloric density of the diet is raised. These neural abnormalities are gradually "corrected" as obesity becomes fully developed, suggesting that obesity is the normal state for such individuals. Thus, defense of the obese body weight may be perpetuated by the formation of new neural circuits involved in energy-homeostasis pathways that are not then easily abolished. Such neural plasticity can occur in both adult life and during nervous-system development. Early pre- and postnatal metabolic conditions (maternal diabetes, obesity, undernutrition) can lead genetically predisposed offspring to become even more obese as adults. This enhanced obesity is associated with altered brain neural circuitry, and these changes can then be passed on to subsequent generations in a feed-forward cycle of ever-increasing body weight. Thus, the metabolic perturbations associated with obesity during both brain development and adult life can produce "metabolic imprinting" on genetically predisposed neural circuits involved in energy homeostasis. Drugs that reduce body weight decrease the defended body weight and alter neural pathways involved in energy homeostasis but have no permanent effect on body weight or neural function in most individuals. Thus, early intervention in mothers, infants, children, and adults 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:Metabolic imprinting on genetically predisposed neural circuits perpetuates obesity. 1105 96

The Fatigue Severity Scale (FSS) is a self-report instrument used to assess levels of fatigue and its effect on daily functioning. The FSS was normed on individuals with multiple sclerosis and has been used in studies examining such factors as obstructive sleep apnea and aerobic exercise. Current research has extended it to obese subjects to assess their level of fatigue in conjunction with a 16-week obesity treatment program. Participants were 118 females with an average age of 45.24 (SD = 11.44). The results yield high pre- and post-test reliability for the FSS and weight loss.
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PMID:Extending the Fatigue Severity Scale to an obese population. 1108 95

alpha, beta, gamma-MSH and ACTH are derived from the same precursor, POMC(proopiomelanocortin), and are classified as melanocortin. alpha-MSH plays an important role in the regulation of appetite and energy expenditure via central melanocortin receptor, melanocortin 4 receptor(MC4R), which is expressed mainly in hypothalamus. alpha-MSH or its analogue shows inhibitory effect on appetite and inversely MC4R antagonist stimulates appetite. MC4R knock-out mice has adult-onset obesity and decreased energy expenditure. POMC gene expression in hypothalamus is partially regulated by leptin. Agouti-related peptide(AgRP), a homologue of agouti peptide and antagonist of MC3R and MC4R, is expressed in human brain and may act as a inhibitor of alpha-MSH. From the genetical aspect, the region near POMC gene, 2p23, is one of the susceptibility loci of human obesity. POMC gene mutations are found in two families, where mutations in both alleles cause human obesity, red hair, adrenal dysfunction, due to alpha-MSH and ACTH deficiencies. In morbidity obese patients, heterozygous MC4R gene mutations are found among 4% of them. These results suggest the importance of melanocortin and its receptors on appetite regulation in human.
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PMID:[Regulation of appetite by melanocortin and its receptors]. 1126 89

Mice lacking NPY Y1 receptors develop obesity without hyperphagia indicating increased energy storage and/or decreased energy expenditure. Then, we investigated glucose utilization in these animals at the onset of obesity. Fasted NPY Y1 knockouts showed hyperinsulinemia associated with increased whole body and adipose tissue glucose utilization and glycogen synthesis but normal glycolysis. Since leptin modulates NPY actions, we studied whether the lack of NPY Y1 receptor affected leptin-mediated regulation of glucose metabolism. Leptin infusion normalized hyperinsulinemia and glucose turnover. These results suggest a possible mechanism for the development of obesity without hyperphagia via dysfunction in regulatory loops involving NPY, leptin and insulin.
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PMID:Increased insulin concentrations and glucose storage in neuropeptide Y Y1 receptor-deficient mice. 1128 97

In males, aging, health and disease are processes that occur over physiologic time and involve a cascade of hormonal, biochemical and physiological changes that accompany the down-regulation of the hypothalamic-anterior pituitary-testicular axis. As aging progresses there are relative increases of body fat and decreases in muscle mass. The increased adipose tissue mass is associated with the production of a number of newly generated factors. These include aromatase, leptin, PAI-1, insulin resistance, and the dyslipidemias, all of which can lead to tissue damage. Fatty tissue becomes the focal point for study as it represents the intersection between energy storage and mobilization. The increase in adipose tissue is associated with an increase in the enzyme aromatase that converts testosterone to estradiol and leads to diminished testosterone levels that favor the preferential deposition of visceral fat. As the total body fat mass increases, hormone resistance develops for leptin and insulin. Increasing leptin fails to prevent weight gain and the hypogonadal-obesity cycle ensues causing further visceral obesity and insulin resistance. The progressive insulin resistance leads to a high triglyceride-low HDL pattern of dyslipidemia and increased cardiovascular risk. All of these factors eventually contribute to the CHAOS Complex: coronary disease, hypertension, adult-onset diabetes mellitus, obesity and/or stroke as permanent changes unfold. Other consequences of the chronic hypogonadal state include osteopenia, extreme fatigue, depression, insomnia, loss of aggressiveness and erectile dysfunction all of which develop over variable periods of time.
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PMID:Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. 1139 22

Males and females both express estrogen receptor (ER) in white adipose tissue (WAT), and estrogens appear to play an important role in regulating WAT in females. However, the role of ER in male WAT was unclear. In this review, we describe our work, which used wild type (WT) and ERalpha-knockout (alphaERKO) male and female mice to determine the role of ERalpha in regulating WAT and brown adipose tissue (BAT). There were progressive increases in WAT with advancing age in alphaERKO compared with WT males; weights of various WAT depots in alphaERKO males were increased by more than 100% compared with WT controls during adulthood. Conversely, BAT weight was similar in alphaERKO and WT males at all ages. Adipocyte areas and numbers were also increased in WAT from alphaERKO compared with WT males. Compared with WT controls, alphaERKO females also had increases in WAT. The alphaERKO mice also had insulin resistance and impaired glucose tolerance, similar to humans lacking ERalpha or aromatase. The obesity in alphaERKO males appeared to involve decreased energy expenditure rather than hyperphagia. In summary, ERalpha absence causes adipocyte hyperplasia and hypertrophy in WAT, but not BAT, and is accompanied by insulin resistance and glucose intolerance in both males and females. These results are the first evidence that the estrogen/ERalpha signaling system is critical in female and male WAT deposition, and may have clinical implications.
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PMID:The role of estrogen and estrogen receptor-alpha in male adipose tissue. 1140 4

Epidemiologic studies have revealed that minimal acute-phase changes predict poor prognoses in many conditions and predict disability and mortality in the elderly. These findings have usually been interpreted to indicate that inflammatory processes of some kind play a role in these situations. In fact, a minimal acute-phase response does not necessarily establish the existence of an inflammatory process but may also reflect a variety of noninflammatory states, including obesity, sleep disturbance, depression, chronic fatigue, and low levels of physical activity. I propose that a minimal acute-phase response may also be a marker of biologic aging, a condition known to predispose to poor prognoses and to death.
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PMID:C-reactive protein elevation can be caused by conditions other than inflammation and may reflect biologic aging. 1140 15

Childhood obesity may be seen as a marker for high-risk dietary and physical inactivity practices. Recent increases in the prevalence of overweight and obesity among American children are not limited to one age, gender, or ethnic group, which suggests that unique behaviors of the members of various racial or ethnic subgroups of the population are unlikely to be the major contributing factors. Rather, it seems that environmental changes promoting increased energy intake and decreased energy output are occurring and have widespread impact on children from various backgrounds. Although no ethnic group is immune from the current shift in energy balance, differential rates of overweight seem to exist among ethnic groups. National probability samples of African-American, Hispanic, and white children in the United States provide clear evidence that white children are at lower risk for childhood overweight than are African-American or Hispanic children. Of concern is the lack of national data on the prevalence of overweight and obesity for Native-American and Asian-American groups. Also of concern is the aggregation of racial and ethnic subgroups, which may render prevalence rates meaningless. This possibility is clearly true with some surveys of weight status that combine diverse populations, such as Asians and Pacific Islanders, into one group. The high rates of obesity in African-American, Hispanic, and Native-American children are of concern. Although parental SES is associated inversely with childhood obesity among whites, higher SES does not seem to protect African-American and Hispanic children against obesity. In these groups, childhood obesity does not seem to be associated significantly with parental income and education. Health consequences of childhood obesity include a higher prevalence of type 2 diabetes and an increased risk for adverse levels of lipids, lipoproteins, and blood pressure. The effects of recently reported unprecedented levels of childhood overweight on subsequent risk for obesity in middle age are not known until future longitudinal data can be collected. It seems likely, however, that future health consequences of current early and severe childhood obesity will be staggering. Funding for adult follow-up of longitudinal studies of high-risk African American, Hispanic, and Native-American children is needed urgently to provide information on the long-term effects of childhood obesity. Halting the obesity epidemic is a formidable task, but the success in recent decades of drastically reducing childhood undernutrition offers hope and should spur similar action and leadership efforts. Promotion of efforts to reduce excess caloric intake with efforts to increase energy expenditure should receive paramount attention in the design of health programs. Given the relatively few published obesity-prevention and treatment studies that are designed to address specific cultural issues, it is important to promote the development of culturally appropriate intervention strategies that are shown to be effective among youth of diverse backgrounds. Although the dietary and activity goals will be similar, parental, family, and community messages and techniques grounded in cultural traditions and norms will be different for each ethnic group. This approach is crucial in the United States, a country with an increasingly diverse population.
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PMID:Ethnic issues in the epidemiology of childhood obesity. 1149 40

The aim of this study was to assess the nature and magnitude of the differences in submaximal and maximal exercise capacity parameters between lean and obese women. A total of 225 healthy obese women 18-65 years (BMI> or=30 kg/m(2)) and 81 non-athletic lean women (BMI< or=26 kg/m(2)) were selected. Anthropometric measurements (weight and height), body composition assessment (bioelectrical impedance method) and a maximal exercise capacity test on a bicycle ergometer were performed. Oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), expired ventilation (VE), respiratory quotient (RQ), breathing efficiency (VE/VO(2)), mechanical efficiency (ME) and anaerobic threshold (AT) were calculated. At a submaximal intensity load of 70 W, VO(2) (l/min) was larger in the obese women and was already 78% of their peak VO(2), whereas in the non-obese it was only 69% (P=0.0001). VE (l/min) was larger, VE/VO(2) did not differ and ME was lower in obese compared to the lean women. AT occurred at the same percentage of peak VO(2) in both lean and obese women. At peak effort, achieved load, terminal VO(2) (l min(-1) kg(-1)), VE, heart rate, RQ respiratory exchange ratio and perceived exertion were lower in obese subjects compared to the non-obese. Obese subjects mentioned significantly more musculoskeletal pain as a reason to end the test, whereas in lean subjects it was leg fatigue. Lean women recovered better as after 2 min they were already at 35% of the peak VO(2), whereas in the obese women it was 47% (P=0.0001). Our results confirm that exercise capacity is decreased in obesity, both at submaximal and peak intensity, and during recovery. Moreover, at peak effort musculoskeletal pain was an important reason to end the test and not true leg fatigue. These findings are important when designing exercise programs for obese subjects.
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PMID:Exercise capacity in lean versus obese women. 1169 16

A progressive decrease in androgen production is common in aging men. The physiological causes for this phenomenon seem to be multifactorial. The magnitude of the decline in testosterone with age and the prevalence of older men with low testosterone levels have not been well established. The extent to which an age-dependent decline in androgen levels leads to health problems that might affect or alter the quality of life remains under debate. In men older than middle age, total testosterone levels may be misleading because of an increase in sex hormone-binding globulin levels. The mechanism of the age-associated decrease of the endocrine testicular function is also essentially due to primary testicular failure, but important changes occur at the hypothalamopituitary level. The most prominent endocrinological alterations with aging are related to the sex steroids, but others, such as growth hormone, melatonin cortisol, and thyroxine, are also affected. The clinical picture of andropause syndrome is characterized by diminished sexual desire and erectile capacity, decrease in intellectual activity, fatigue, depression, decrease in lean body mass, skin alterations, decrease in body hair, decrease in bone mineral density that results in osteoporosis, and increase in visceral fat and obesity. Current medical treatments for androgen supplementation include oral tablets, intramuscular injections, and scrotal and nonscrotal patches. Unfortunately, none of these preparations mimic the circadian rhythm, even if some of them may approximate the circadian rhythm by dose adjustments. Moreover, the androgen supplementation could have adverse effects on different organs, namely, the liver, lipid profile, cardiovascular disease, prostate, sleep disorders, and emotional behavior. Clinical response is a better guide to dose requirements, regardless of serum testosterone levels. This important field must be actively investigated by the medical, behavioral, and social sciences.
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PMID:Male andropause: myth, reality, and treatment. 1215 25


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