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

A 28-year-old mentally retarded, institutionalised woman was referred to us for evaluation of multiple plantar warts and ingrown nails of both great toes. The patient was born to unrelated parents of North African origin and had one brother and three half-brothers, all of whom were healthy. Physical examination revealed short stature, slight obesity, facial abnormalities (Fig. 1), short and broad thumbs and big toes (Figs. 2 and 3). A keloid was found on the right forearm, that had developed after surgical correction of a fracture (Fig. 4). Ill-defined hyperpigmented macules were observed on the trunk. The patient also presented pruritic eczematous lesions of the limbs and the back that had been present for some years and were recurrent despite treatment with emollients and local steroids. Androgenetic-type alopecia of moderate severity was seen on the vertex of the scalp. Past medical history included polydactylism of the feet and clinodactyly of the thumbs (both corrected surgically), respiratory tract infections, Wolf-Parkinson-White syndrome and refractive errors necessitating glasses.
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PMID:Clinical quiz. Rubinstein-Taybi syndrome (synonyms: broad thumbs and great toes, characteristic facies, and mental retardation -- broad thumb-hallux syndrome). 1180 12

Inadequate pharmacological tools, until recently, hindered the understanding of the roles of corticotropin-releasing factor (CRF) receptor subtypes in appetite regulation and gastrocolonic motor function. Now, novel ligands that are selective for CRF(1) or CRF(2) receptors are helping to uncover the specific functions of CRF receptor subtypes. Central or peripheral CRF(2) receptor activation suppresses feeding independently of CRF(1) receptors. In the rat, central administration of CRF(2) receptor agonists promotes satiation without eliciting the malaise, behavioral arousal or anxiogenesis associated with CRF(1) receptor agonists. Conversely, central administration of CRF(1) receptor agonists elicits short-onset anorexia independently of CRF(2) receptor activation. With respect to gastrointestinal motor function, stress inhibits gastric motility through CRF(2) receptor-dependent central autonomic and peripheral myenteric systems. By contrast, stress stimulates colonic motility via CRF(1) receptor-dependent sacral parasympathetic and colonic myenteric mechanisms. These findings have important physiological implications and suggest targeted approaches for the pharmacotherapy of obesity and stress-related functional gastrointestinal and eating disorders.
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PMID:Nibbling at CRF receptor control of feeding and gastrocolonic motility. 1291 52

The present study reports a rare case of full-blown Cushing's disease several years after an episode of pituitary apoplexy. A 60 year-old woman complained of muscular weakness and generalized malaise. Ten years ago she had an episode of pituitary apoplexy. Diabetes mellitus was diagnosed at age 56, and thereafter she had been controlled her plasma glucose with diet therapy and oral hypoglycemic agents. She exhibited cushingoid feature of moon face and central obesity. Both plasma ACTH and serum cortisol levels were elevated to 170 pg/ml and 19.6 microg/dl, respectively. Dexamethasone suppression test showed that a large dose of 8 mg dexamethasone, but not a small dose of 2 mg, suppressed the pituitary-adrenocortical axis. CRH and methyrapone caused increases in plasma ACTH and serum cortisol levels. Brain T(1)-weighted magnetic resonance imaging depicted a low signal of pituitary tumor, which was not enhanced by gadolinium. The pituitary tumor was removed by transsphenoidal adenomectomy, and immunohistochemistry revealed an ACTH-producing adenoma. The evidence suggested the possibility that the two pituitary tumors with dormant period of several years were a recurrence of ACTH-producing tumors in the present patient.
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PMID:Full-blown Cushing's disease after an episode of pituitary apoplexy. 1461 5

NAFLD/NASH is now recognised as an increasing clinical problem in children and adolescents. Risk factors include obesity, insulin resistance, and hypertriglyceridaemia. Drug hepatoxicity and genetic or metabolic diseases that can cause hepatic steatosis must be excluded. Affected children are usually asymptomatic although a few may complain of malaise, fatigue, or vague recurrent abdominal pain. Liver biopsy is the gold standard for diagnosis, and is important in determining disease severity and prognosis. The natural history of childhood NASH may be progressive liver disease for a significant minority. Long term follow up studies in this population are still lacking. The mainstay of treatment is weight reduction. The use of pharmacological therapy, though promising, ideally needs further evaluation in well designed randomised controlled studies in children.
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PMID:Fatty liver disease in children. 1521 Apr 98

The aetiology of chronic fatigue syndrome (CFS) is unknown; however, recent evidence suggests excessive free radical (FR) generation may be involved. This study investigated for the first time levels of 8-iso-prostaglandin-F(2 alpha)-isoprostanes alongside other plasma markers of oxidative stress in CFS patients and control subjects. Forty-seven patients (18 males, 29 females, mean age 48 [19--63] years) who fulfilled the Centres for Disease Control classification for CFS and 34 healthy volunteers (13 males, 21 females, 46 [19--63] years) were enrolled in the study. The CFS patients were divided into two groups; one group had previously defined cardiovascular (CV) risk factors of obesity and hypertension (group 1) and the second were normotensive and nonobese (group 2). Patients had significantly increased levels of isoprostanes (group 1, P=0.007; group 2, P=0.03, unpaired t test compared to controls) and oxidised low-density lipoproteins (group 2, P=0.02) indicative of a FR attack on lipids. CFS patients also had significantly lower high-density lipoproteins (group 1, P=0.011; group 2, P=0.005). CFS symptoms correlated with isoprostane levels, but only in group 2 low CV risk CFS patients (isoprostanes correlated with; total symptom score P=0.005; joint pain P=0.002; postexertional malaise P=0.027, Pearson). This is the first time that raised levels of the gold standard measure of in vivo oxidative stress (isoprostanes) and their association with CFS symptoms have been reported.
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PMID:Oxidative stress levels are raised in chronic fatigue syndrome and are associated with clinical symptoms. 1608 77

Apolipoprotein E (apoE) isoforms have different affinity to lipoprotein (LP) receptors and lipids. In comparison with the "normal" apoE3 the apoE2 affinity to receptors is strictly decreased influencing its association with hypoholesterolemia and accumulation of LP of very-low density in the plasma. The apoE4 is characterized by the increased affinity to LP receptors and is associated with hyperholesterolemia (HCHL). In the homozygotes on allele E2 the gender, age, obesity, diabetes and some other factors have an influence on conversion of hypoholesterolemia to type Ill hyperlipidemia. The ApoE4 association with HCHL may be due to its impaired recycling in hepatocytes. The ApoE isoforms influence the hypolipidemic therapy efficacy: statins and physical training were more effective in epsilon2 allele carriers and probucol and low-fat diet had the maximal effect in epsilon4 allele carriers.
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PMID:[The role of epsilon 2/epsilon 3/epsilon 4 polymorphism of the apolipoprotein E gene in the development of dislipoproteinemia and its influence on the efficacy of the hypolipidemic therapy]. 1724 78

Based on the Body Mass Index (BMI, kg/m(2)), most men in nations such as the UK and USA are reportedly overweight or obese. This is authoritatively defined as a massive and growing problem. Drawing from embodied sociology, critical obesity literature and qualitative data generated during an Economic and Social Research Council funded project on masculinities and weight-related issues, this paper offers a critical realist contribution to the obesity debate. Rather than endorsing the institutionalised war on fat, and correcting so-called 'laymen' who dismiss medicalized weight-for-height recommendations, the following presents and honours men's justificatory accounts for levels of body mass that medicine labels too heavy (implicitly or explicitly too fat). Men's critical understandings, which are connected to their displays of moral worth, are considered under three headings: the compatibility of heaviness, healthiness and physical fitness; looking and feeling ill at a supposedly 'healthy' BMI; and resisting irrational standardisation. By empirically 'bringing in' men's meanings, sensibilities and culturally informed aesthetics, this paper casts a different light on medicalized measures that support potentially corrosive obesity epidemic psychology.
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PMID:Body Mass Index, masculinities and moral worth: men's critical understandings of 'appropriate' weight-for-height. 1749 70

Circulating levels of the cytokine interleukin 18 (IL-18) are elevated in obesity. Here, we show that administration of IL-18 suppresses appetite, feed efficiency, and weight regain in food-deprived male and female C57BL/6J mice. Intraperitoneal vs. intracerebroventricular routes of IL-18 administration had similar potency and did not promote formation of a conditioned taste aversion (malaise-like behavior). Mice partially (Il18(+/-)) or totally (Il18(-/-)) deficient in IL-18 were hyperphagic by young adulthood, with null mutants then becoming overweight by the fifth month of life. Adult Il18(-/-) mice gained 2- to 3-fold more weight than WT mice per unit energy consumed of low- or high-fat diet. Indirect calorimetry revealed reduced energy expenditure in female Il18(-/-) mice and increased respiratory exchange ratios [volume of carbon dioxide production (VCO(2))/volume of oxygen consumption (VO(2))] in mutants of both sexes. Hyperphagia continued in maturity, with overeating greatest during the mid- to late-dark cycle. Relative white fat-pad mass of Il18(-/-) mice was approximately 2- to 3-fold greater than that of WT, with gonadal, mesenteric, and inguinal depots growing most. The data suggest that endogenous IL-18 signaling modulates food intake, metabolism, and adiposity during adulthood and might be a central or peripheral pharmacological target for controlling energy homeostasis.
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PMID:Interleukin-18 controls energy homeostasis by suppressing appetite and feed efficiency. 1757 27

Heat stroke in athletes is entirely preventable. Exertional heat illness is generally the result of increased heat production and impaired dissipation of heat. It should be treated aggressively to avoid life-threatening complications. The continuum of heat illness includes mild disease (heat edema, heat rash, heat cramps, heat syncope), heat exhaustion, and the most severe form, potentially life-threatening heat stroke. Heat exhaustion typically presents with dizziness, malaise, nausea, and vomiting, or excessive fatigue with accompanying mild temperature elevations. The condition can progress to heat stroke without treatment. Heat stroke is the most severe form of heat illness and is characterized by core temperature >104 degrees F with mental status changes. Recognition of an athlete with heat illness in its early stages and initiation of treatment will prevent morbidity and mortality from heat stroke. Risk factors for heat illness include dehydration, obesity, concurrent febrile illness, alcohol consumption, extremes of age, sickle cell trait, and supplement use. Proper education of coaches and athletes, identification of high-risk athletes, concentration on preventative hydration, acclimatization techniques, and appropriate monitoring of athletes for heat-related events are important ways to prevent heat stroke. Treatment of heat illness focuses on rapid cooling. Heat illness is commonly seen by sideline medical staff, especially during the late spring and summer months when temperature and humidity are high. This review presents a comprehensive list of heat illnesses with a focus on sideline treatments and prevention of heat illness for the team medical staff.
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PMID:Heat-related illness in athletes. 1760 28

Hypothalamic obesity, or intractable weight gain after hypothalamic damage, is one of the most pernicious and agonizing late effects of CNS insult. Such patients gain weight even in response to caloric restriction, and attempts at lifestyle modification are useless to prevent or treat the obesity. The pathogenesis of this condition involves the inability to transduce afferent hormonal signals of adiposity, in effect mimicing a state of CNS starvation. Efferent sympathetic activity drops, resulting in malaise and reduced energy expenditure, and vagal activity increases, resulting in increased insulin secretion and adipogenesis. Pharmacologic treatment is difficult, consisting of adrenergics to mimick sympathetic activity, or suppression of insulin secretion with octreotide, or both. Recently, bariatric surgery (Roux-en-Y gastric bypass, laparoscopic gastric banding, vagotomy) have also been attempted with variable results. Early and intensive management is required to stave off the obesity and its consequences.
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PMID:Hypothalamic obesity: causes, consequences, treatment. 1920 8


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