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

Glucocorticoids have a broad array of life-sustaining functions and play an important role in the therapy of many diseases. Thus, changes of tissue sensitivity to glucocorticoids may be associated with and influence the course and treatment of many pathologic states. Such tissue sensitivity changes may present on either side of an optimal range, respectively as glucocorticoid resistance or hypersensitivity, and may be generalized or tissue-specific. Familial/sporadic glucocorticoid resistance syndrome caused by inactivating mutations of the glucocorticoid receptor (GR) gene is a classic monogenic disorder associated with congenital, generalized glucocorticoid insensitivity, while several autoimmune, inflammatory and allergic diseases are often associated with resistance of the inflamed tissues to glucocorticoids. On the other hand, glucocorticoid hypersensitivity has been suggested in visceral obesity-related insulin resistance associated with components of the metabolic syndrome, and in the acquired immunodeficiency syndrome (AIDS) caused by human immunodeficiency virus type-1 (HIV-1) infection. Here, we have reviewed the molecular analyses of five familial and three sporadic cases of the familial/sporadic glucocorticoid resistance syndrome and discussed the possible contribution of newly identified molecules, such as HIV-1 accessory proteins Vpr and Tat, FLICE-associated huge protein (FLASH) and chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII), on the molecular regulation of GR activity, as well as their possible contribution to changes in tissue sensitivity to glucocorticoids in pathologic conditions.
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PMID:Tissue glucocorticoid resistance/hypersensitivity syndromes. 1294 36

The obesity crisis in the United States has been associated with an alarming increase in the prevalence of the metabolic syndrome (MSX) disease cluster. Here we review evidence that the MSX reflects a failure of a system of intracellular lipid homeostasis that prevents lipotoxicity in the organs of overnourished individuals by confining the lipid overload to cells specifically designed to store large quantities of surplus calories, the white adipocytes. Normally, early in obesity, adipocytes increase leptin and adiponectin secretion, hormones that enhance oxidation of surplus liquids in nonadipose tissues by activating AMP-activated protein kinase and reducing the activity and expression of lipogenic enzymes. These events combine to lower malonyl coenzyme A. Deficiency of and/or unresponsiveness to leptin prevents these protective events and results in ectopic accumulation of lipids. Increased de novo ceramide formation is probably the most damaging lipid and is a cause of lipoapoptosis, abetted by a decline in tissue Bcl-2. Pancreatic beta-cells and myocardiocytes are cellular victims of the process, leading to non-insulin-dependent diabetes and lipotoxic cardiomyopathy. The MSX is particularly prevalent in visceral obesity, probably because visceral adipocytes make less leptin than sc adipocytes. Cushing's syndrome, the lipodystrophy associated with protease inhibitor therapy of AIDS, polycystic ovarian disease, as well as diet-induced visceral obesity, all have a high waist/hip ratio, and all exhibit MSX. Increased lipid content in the heart and skeletal muscle organs of such patients is now under study.
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PMID:Minireview: weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome. 1296 11

The life-stage approach, which views the behaviours and exposures of an individual from the preconceptual situation of the parent through pregnancy, infancy, childhood and adolescence, and into the advancing years through adulthood, is the basis of analysis of strategies to improve long-term health. Among the behaviours of note is the dietary selection pattern, conditioning our exposure to nutrients and dietary constituents that influences growth, nutriture, cognitive and physical performance, and disease resistance and susceptibility. The African Diaspora created a population displaced from Africa to the Western Hemisphere as part of the African slave trade from the 16th to 18th centuries. It continues to manifest distinct dietary and lifestyle practices in the context of a health experience that is different both from the population in their African countries of origin and from the other ethnicities in their countries of displacement and current residence. Afro-Americans are more susceptible to a series of diseases and conditions including low birth weight, violence, and HIV/AIDS, as well as the non-communicable diseases: obesity, diabetes mellitus, cardiovascular disease, hypertension, stroke, renal failure, breast cancer, prostate cancer and lead poisoning. The differential nature of dietary practices are conditioned at times by the poverty and marginalisation of the populace, resulting in either disadvantageous or beneficial outcomes relative to others' eating habits. Serious consideration must be given to the possibility that ethnic difference give rise to different requirements and tolerances for essential nutrients and distinct protective or adverse responses to foods and dietary substances. The major challenges to health improvement for the African Diaspora is coming to grips with the policy and programmatic nuances of differential treatment and the effecting the behavioural changes that would be needed in a population skeptical of the motives of media and of the power elites of their societies.
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PMID:Diet and long-term health: an African Diaspora perspective. 1450 96

In this paper the perspective for nutritional modulation of systemic impairment in patients with chronic obstructive pulmonary disease (COPD) is discussed. Progressive weight loss is characterised by disease-specific elevated energy requirements unbalanced by dietary intake. Weight gain per se can be achieved by caloric supplementation while future studies may prove efficacy of amino acid modulation to stimulate protein synthesis and enhance muscle anabolism. Disproportionate muscle wasting resembles the cachexia syndrome as described in other chronic wasting diseases (cancer, chronic heart failure, acquired immunodeficiency syndrome (AIDS)). There is yet no adequate nutritional strategy available to treat cachexia in COPD. Muscle substrate metabolism has hardly been investigated, but the few data available point towards a decreased fat oxidative capacity that may show similarities with the "metabolic syndrome" as described in type II diabetes and obesity and could theoretically benefit from polyunsaturated fatty acid modulation. To adequately target the different therapeutic options, clearly more clinical (intervention) studies are needed in chronic obstructive pulmonary disease patients that are adequately characterised by local and systemic impairment and in which molecular and metabolic markers are linked to functional outcome.
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PMID:Nutritional and metabolic modulation in chronic obstructive pulmonary disease management. 1462 Nov 10

The United States is the epicenter of an obesity pandemic. As more countries acculturate to a Western lifestyle, rates of obesity and its sequelae are rising steadily in both adults and children. In response, a variety of weight-loss diets emphasizing alternative distributions of macronutrient classes have been promoted with considerable success. Among the most popular is the so-called "Atkins Diet," in which carbohydrate restriction is touted as the key to weight loss. Despite claims, however, evidence that weight loss is enhanced by means other than caloric restriction is lacking. Also lacking is evidence that fad diets produce sustainable weight loss. Most important, fad diets generally ignore or refute what is known about fundamental associations between dietary pattern and human health. Cancer, cholera, and AIDS induce rapid weight loss, highlighting the potential incompatibility of weight loss by any means with health. Available data suggest that long-term weight loss is most consistently achieved by adherence to a fat-restricted diet abundant in grains, vegetables, and fruit, along with regular physical activity, a lifestyle notably conducive to the promotion of overall health. Fad diets, potential harms of which are well characterized, should be presumed "guilty" of incompatibility with human health until or unless proved otherwise; the burden of proof should reside with proponents. In the interim, the clinical and public health communities should work to empower individuals with knowledge needed to reconcile weight control with health promotion; support policies that mitigate obesogenic environmental conditions; and offer unified resistance to the contagion of dietary propaganda.
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PMID:Pandemic obesity and the contagion of nutritional nonsense. 1465 42

Body composition has become the main outcome of many nutritional intervention studies including osteoporosis, malnutrition, obesity, AIDS, and aging. Traditional indirect body composition methods developed with healthy young adults do not apply to the elderly or diseased. Fast neutron activation (for N and P) and neutron inelastic scattering (for C and O) are used to assess in vivo elements characteristic of specific body compartments. Non-bone phosphorus for muscle is measured by the (31)P(n, alpha)(28)Al reaction, and nitrogen for protein via the (14)N(n,2n)(13)N fast neutron reaction. Inelastic neutron scattering is used to measure total body carbon and oxygen. Body fat is derived from carbon after correcting for contributions from protein, bone, and glycogen. Carbon-to-oxygen ratio (C/O) is used to measure the distribution of fat and lean tissue in the body and to monitor small changes of lean mass. A sealed, D-T neutron generator is used for the production of fast neutrons. Carbon and oxygen mass and their ratio are measured in vivo at a radiation exposure of less than 0.06 mSv. Gamma-ray spectra are collected using large BGO detectors and analyzed for the 4.43 MeV state of carbon and 6.13 MeV state of oxygen, simultaneously with the irradiation. P and N analysis by delayed fast neutron activation is performed by transferring the patient to a shielded room equipped with an array of NaI(Tl) detectors. A combination of measurements makes possible the assessment of the "quality" of fat-free mass. The neutron generator system is used to evaluate the efficacy of new treatments, to study mechanisms of lean tissue depletion with aging, and to investigate methods for preserving function and quality of life in the elderly. It is also used as a reference method for the validation of portable instruments of nutritional assessment.
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PMID:Use of D-T-produced fast neutrons for in vivo body composition analysis: a reference method for nutritional assessment in the elderly. 1474 91

Adiponectin (also called AdipoQ, gelatin-binding protein 28, Acrp30) is a novel adipocytokine with important metabolic effects. It is physiologically released from adipose tissue and circulates in serum as a hexamer and larger multimeric structure of high molecular weight. Serum level of the protein correlates with systemic insulin sensitivity. Recently adiponectin receptors AdipoR1 and AdipoR2 have been discovered by expression cloning. AdipoR1 is abundantly expressed in skeletal muscles, whereas AdipoR2 is predominantly expressed in the liver. Marked expression of mRNA for AdipoR1 and AdipoR2 has been lately reported in pancreatic beta cells. Both of the receptors activate AMPK and PPAR alpha metabolic pathways leading to an increase in fatty acid oxidation, glucose uptake and a decreased rate of gluconeogenesis, thus enhancing insulin sensitivity. Moreover effects of adiponectin mimic many metabolic actions of insulin such as augmenting blood flow and glucose disposal in NO-dependent manner. The precise mechanism of regulation of plasma adiponectin level is unknown. Recently the mechanism of transcriptional activation of adiponectin gene via PPAR gamma was described. Its level seems to be decreased by TNFalfa and beta-adrenergic agonists. Furthermore there is increasing evidence that some genetic variants in the adiponectin gene may be associated with its ethnical differences in level as well as its likely clinical consequences. Hipoadiponectynemia is associated with obesity, metabolic syndrome, diabetes type 2, cardiovascular disease, lipodystrophy in AIDS. In patients with chronic renal failure, anorexia nervosa plasma adlponectin level is increased. Weight loss and therapy with thlazolidinediones are proved to enhance endogenous adlponectin production in humans. In summary, the ability of adiponectin to increase insulin sensitivity in conjunction with its anti-inflammatory and antiatherogenic properties have made this novel adipocytokine a promising therapeutic tool for the future, especially in individuals with low plasma levels of adiponectin.
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PMID:[Adiponectin--adipocytokine with a broad clinical spectrum]. 1523 Jan 53

An increase in the mycotic infections has been observed in recent decades. It is the effect of the development of industry, large migrations, living in huge aglomerations, usage of the public swimming-pools, wearing impervious clothes and shoes. Systemic diseases: diabetes, obesity, hormonal disorders, immune and food deficiency, AIDS, neoplasms and prescription drugs: antibiotics, corticosteroids and immunosuppressants, cause mycoses. Mycoses belong to chronic diseases, they are difficult to treat and very often recur. A lot of antimycotic drugs are known, but the most effective are azoles and alliloamines. An intensive research is conducted on introduction of new and more effective and cheaper preparations.
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PMID:Mycoses--prophylaxis and treatment. 1532 86

In maintenance hemodialysis (MHD) patients, associations between demographic, clinical and laboratory values and mortality, including cardiovascular death, are significantly different and, in some cases, in the opposite direction of those derived from the general population. This phenomenon, termed 'reverse epidemiology', is not limited to MHD patients but is also observed in populations that encompass an estimated 20 million Americans including those with an advanced age, heart failure, malignancies, and AIDS. A significant portion of this reversal may be due to the overwhelming effect of the malnutrition-inflammation complex syndrome (MICS). Since two thirds of MHD patients die within 5 years of initiation of dialysis treatment, traditional cardiovascular risk factors such as obesity, hypercholesterolemia and hypertension cannot exert a long-term deleterious impact, and instead, their short-term beneficial effects on MICS provides a survival advantage. In order to improve survival and quality of life in MHD patients, extrapolated ideal norms derived from the general population should be substituted with novel norms obtained from outcome-oriented epidemiologic analyses while accounting for the differential effect of MICS in different case-mix subgroups.
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PMID:Reverse epidemiology: a spurious hypothesis or a hardcore reality? 1562 38

Epidemiology in the past was concerned essentially by the study of infectious diseases which were the cause of huge mortalities especially since urbanisation was initiated. Epidemics of pest, typhus, cholera, influenza a.o. were common. The epidemics were halted by better hygiene, vaccination and antibiotics. Since the second world war epidemiology was dominated by an "epidemic" of new chronic diseases, especially heart disease and cancer. This was due to an increase in life span and to an increase in smoking habits and in the intake of saturated fat and a too small intake of fruit and vegetables combined with a too high intake of salt (NaCl). Gradually epidemiology evolved as the study of the causes, the distribution, the risk factors and the prevention of chronic diseases, but also including accidents, suicide, depression a.o., diseases with a mass occurrence at the population level. The importance of nutrition as a determinant of health gradually became recognized, but remains undervalued by the medical profession. Mortality at the population level follows some simple mathematical laws and can be represented accurately (r2>0.99) between the ages of 35 and 84 year by either Gompertz equations (ln mortality versus age) or by a polynomial equation (ln mortality versus age, age2). This is valid for all populations and both sexes and remains valid at times of great and rapid changes in mortality. This shows that measures for prevention should be directed towards the total population. The future of epidemiology should be directed towards the slowing of the ageing process at the population level by a healthy life style consisting of: not smoking, avoiding obesity, a fair amount of physical activity and a healthy nutrition i.e little salt, little saturated fat, an adequate amount of omega-3 fatty acids and a large amount of fruit and vegetables, with an occasional glass of red wine. This contains the secret of a long and healthy life. Conceptually it will be important to determine whether a maximum human life span, genetically determined, exists. A maximal rectangularization of the mortality curve should then be the ultimate goal. At the same time the possible re-emergence of old and new infectious diseases (SARS, Ebola, BSE, AIDS) should be kept in mind.
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PMID:Epidemiology: past, present and future. 1564 67


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