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

Cardiovascular disease (CVD), and in particular coronary artery heart disease (CAHD), is the leading cause of morbidity and mortality in women. Until recently, most of our knowledge about the pathophysiology of CVD in women - and, subsequently, management guidelines - were based on studies conducted mostly in men. While similar mechanisms operate to induce CVD in women and men, gender-related differences exist in the anatomy and physiology of the myocardium, and sex hormones modify the course of disease in women. Women, more than men, have their initial manifestation of CAHD as angina pectoris; are likely to be referred for diagnostic tests at a more advanced stage of disease, and are less likely than men to have corrective invasive procedures. The overall morbidity and mortality following the initial ischaemic heart event is worse in women, and the case fatality rate is greater in women than in men. Also, the relative impact of impaired vasoreactivity of the coronary artery, increased viscosity of the blood and dysregulation of automaticity and arrhythmia, is greater in women than in men. The most effective means of decreasing the impact of CVD on women's health is by an active approach from childhood to proper principles of healthcare in order to modify the contribution of specific risk factors. The latter include obesity, abnormal plasma lipid profile, hypertension, diabetes mellitus, cigarette smoking, sedentary lifestyle, increased blood viscosity, augmented platelet aggregability, stress and autonomic imbalance. The use of lipid-lowering drugs has not been adequately studied in women but reports from studies conducted mostly in men do predict an advantage also to women. Oestrogen deficiency after spontaneous or medically induced menopause is an important risk factor for CVD and CAHD. Observational and mechanistic data suggest a role for oestrogen replacement after menopause for primary, and possibly secondary, prevention of CVD. However, two recent prospective trials suggest that treatment de novo with hormone replacement of older post-menopausal women after an acute coronary event may not confer cardiovascular protection and may increase the risk of thromboembolic disease. Results of ongoing long-term studies may determine the beneficial role of hormone replacement versus potential risks involved with this treatment.
Best Pract Res Clin Obstet Gynaecol 2002 Jun
PMID:Update on cardiovascular disease in post-menopausal women. 1209 66

The effect of weight, classified by body mass index (BMI), on bone mass (BMC) of the whole body and on bone mineral density BMD of the hip joint was analysed in a sample of 120 Austrians of Vienna and surroundings. The 68 females and 52 males of this cross sectional study ranged in age between 60 and 92 years (x = 71.7 +/- 7.7). Age distribution was not significantly different between sexes. The WHO (1997) classification of body mass index (BMI) was used for weight classification, i.e. normal weight (BMI 18.5-24.99) and moderate overweight (BMI 25.0-29.99). Obese subjects (BMI 30+) were not included in this study. Bone mass of the whole body as well as bone density of the hip joint were determined by Dual-energy-X-ray absorptiometry (DEXA) using a hologic 2000 scanner. As expected BMC and BMD values were significantly higher in males than in females. While in both females and males moderately overweight BMD of the hip was significantly higher than in those with normal BMI, statistically significant differences of BMC were restricted to females only. Such positive association between body weight and BMC and BMD is in agreement with previous studies on mature subjects, and menopausal and postmenopausal women in particular. In addition, this study demonstrates corresponding positive associations between moderate overweight and bone mass and -density in the elderly and old aged.
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PMID:Protective effect of moderate overweight on bone density of the hip joint in elderly and old Austrians. 1216 64

Understanding the pathogenesis of non-alcoholic steatohepatitis has recently assumed great importance with the recognition that it has the potential to progress to fibrosis and cirrhosis. The 'two-hit' model of pathogenesis was proposed in 1998, with the first 'hit' - steatosis - increasing the sensitivity of the liver to the second 'hits' mediating liver injury. The main aim of this chapter is to review this model in the light of studies that have been published over the subsequent 4 years. Particular attention will be focused on the role of insulin resistance and recent advances in our understanding of the basic cellular mechanisms linking obesity and insulin resistance. Based on this information I will propose a modification of the two-hit model that places more emphasis on the role of free fatty acids. This model will provide the basis for further research and enable the rational design of treatment strategies.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Pathogenesis of steatohepatitis. 1240 38

Nonalcoholic steatohepatitis (NASH), which is the most severe histological form of nonalcoholic fatty liver disease (NAFLD), is emerging as the most common clinically important form of liver disease in developed countries. Although its prevalence is 3% in the general population, this increases to 20-40% in obese patients. Since NASH is associated with obesity, prevalence has been predicted to increase along with the arsent epidemic of obesity and type II diabetes mellitus. The importance of this observation comes from the fact that NASH is a progressive fibrotic disease, in which cirrhosis and liver-related death occur in 25% and 10% in these patients respectively over a 10-year period. This is of particular concern given the increasing recognition of NASH in children. Treatment consists of treating obesity and its co-morbidities; diabetes and hyperlipidemia. Nascent studies suggest that a number of pharmacological therapies may be effective, but all remain unproven at present. Histological and laboratory improvement occurs with a 10% decrease in body weight. Bariatric surgery is indicated in selected patients.A greater understanding of the pathophysiological progression of NASH in obese patients must be obtained in order to develop more focused and improved therapy.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Steatohepatitis in obese individuals. 1240 42

Steatohepatitis in children occurs in the childhood version of non-alcoholic fatty liver disease (NAFLD), as a result of hepatotoxicity and with certain genetic/metabolic diseases. Until recently, NAFLD was considered to be rare in children. It is now recognized as an important childhood liver disease, especially because childhood obesity is much more common. Children with NAFLD may present as young as 4 years old; males tend to predominate; fibrosis is often found on liver biopsy and cirrhosis has been reported. Treatment for childhood NAFLD currently consists of weight reduction plus regular aerobic exercise; vitamin E may be an effective adjunctive therapy. Drug hepatotoxicity and genetic/metabolic diseases that can cause fatty liver, such as Wilson's disease and cystic fibrosis, must be excluded since treatment is radically different. Other causes of chronic hepatitis, such as chronic viral hepatitis, must also be excluded. Multisystemic inherited diseases with hyperinsulinaemia plus insulin resistance may have NAFLD as hepatic involvement and should be identified.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Steatohepatitis in children. 1240 43

Obesity-related steatosis is an increasingly common histological finding in liver biopsies and may co-exist with other chronic liver diseases. Although non-alcoholic fatty liver disease (NAFLD) without true steatohepatitis is generally a benign condition, when another liver disease is present, steatosis may exacerbate the liver damage. In this review, we discuss the interaction of obesity-related steatosis with chronic hepatitis C, alcoholic liver disease, disorders of hepatic iron storage and drug-induced liver disease. The role of weight reduction in minimizing liver injury in patients with chronic hepatitis C is discussed. Finally, we discuss the problems associated with orthotopic liver transplantation for patients with NAFLD.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Interaction of non-alcoholic fatty liver disease with other liver diseases. 1240 44

Non-alcoholic fatty liver disease (NAFLD) is usually seen in middle-aged women with obesity, non-insulin-dependent diabetes mellitus and/or hyperlipidaemia. NAFLD has also been associated with other conditions. Surgical procedures to treat obesity such as jejunoileal bypass and gastroplasty as well as massive small bowel resection have been associated with NAFLD. Mechanisms such as rapid weight loss, certain nutritional deficiencies and bacterial overgrowth have been proposed. Other nutritional conditions such as extreme malnutrition and total parenteral nutrition can also cause NASH. This can be due to abnormal glucose and fat metabolism, deficiencies like carnitine, essential fatty acid and choline or, in the case of parenteral nutrition, excess of calories, glucose or lipids. Several drugs have also been implicated as well as some inborn errors of metabolism and, more rarely, other diseases.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Other disease associations with non-alcoholic fatty liver disease (NAFLD). 1240 45

Treatment of patients with non-alcoholic steatohepatitis (NASH) has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipidaemia. NASH associated with obesity may resolve with weight reduction, although the benefits of weight loss have been inconsistent. Appropriate control of glucose and lipid levels is always recommended, but is not always effective in reversing the liver condition. Results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, alpha-tocopherol, metformin and thiazolidinedione derivatives suggest that these medications may be of potential benefit for patients with NASH. These medications, however, need first to be tested in well-controlled trials with clinically relevant end-points and extended follow-up. A better understanding of the pathogenesis and natural history of NASH will help to identify the subset of patients at risk of progressing to advanced liver disease and, hence, those patients who should derive the most benefit from medical therapy.
Best Pract Res Clin Gastroenterol 2002 Oct
PMID:Treatment of non-alcoholic steatohepatitis. 1240 46

Obesity can be defined as the excessive accumulation of fat in adipose tissue, to the extent that health may be impaired. The most widely used measures of total and abdominal adiposity are the body mass index and waist circumference. Obesity is now a global public health problem, with about 315 million people world-wide estimated to fall into the WHO-defined obesity categories with a body mass index (BMI) of 30 or above. The primary causes of the rapid global rise in obesity rates lie in the profound environmental and societal changes now affecting large parts of the world and creating societies in which physical activity is low and the availability of high-fat, energy-dense foods has increased. Strategies aimed at preventing weight gain and obesity have not been successful to date but are likely to be more cost effective, and to have a greater positive impact on long-term control of body weight than treating obesity once it has developed.
Best Pract Res Clin Endocrinol Metab 2002 Dec
PMID:Obesity: epidemiology and possible prevention. 1246 9

It has been a little more than 5 years since the publication of the first genome scans focused on obesity-related phenotypes in humans. While the number of scans reported has grown steadily during this time, the results from many of these studies have been modest at best. However, there are a handful of studies that have now reported highly significant findings, and even more important perhaps is the fact that several of these findings have now been replicated as well. Currently there is strong statistical support for approximately half a dozen quantitative trait loci (QTLs) influencing obesity-related phenotypes across a number of populations and ethnic groups. While some of these signals localize near genes that might have been considered a priori as candidate genes for obesity, several others offer evidence for previously unsuspected genes. As a result, there is an intriguing pattern of genetic contribution to obesity that has begun to emerge and which promises to greatly increase our understanding of the relationship between obesity and other chronic diseases such as coronary heart disease and type 2 diabetes.
Best Pract Res Clin Endocrinol Metab 2002 Dec
PMID:The emerging pattern of the genetic contribution to human obesity. 1246 10


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