Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, interest has tended to focus on prevention of coronary events in high-risk groups, particularly those with established coronary heart disease. While this is understandable, it has led to a lack of emphasis on primary prevention. Yet it is only by means of primary or even pri-mordial prevention that a substantial reduction in coronary mortality on a population level will be achieved. This becomes clear when we consider that half of all persons who suffer a first myocardial infarction will die within the first month thereafter. Nevertheless, major progress has been made in primary prevention. Reliable risk algorithms have been constructed in Europe (PROCAM) and the U.S., and preliminary analyses on both sides of the Atlantic indicate that these algorithms can be useful applied to populations which are geographically and ethnically distinct from those in which they were derived. A notable trend in recent years is the increasing recognition of the metabolic syndrome with its key components of abdominal obesity, hypertriglyceridemia hypertension, low HDL-C, small, dense LDL, insulin resistance and hyperinsulinemia as being perhaps the most common and dangerous metabolic abnormality of all. Newer risk markers are being evaluated. The position of homocysteine remains unclear. Despite a strong association of elevated homocysteine with risk in case-control studies, prospective investigations have been less convincing. Evidence is beginning to accumulate from cross-sectional and prospective studies that markers of inflammation such as C-reactive peptide may improve our ability to predict risk of coronary events. While these data are encouraging, results of further studies must be awaited before the true place of these markers can be determined. The same can be said of many genetic markers of risk. Though a very large number of association studies have indicated links between a variety of genetic markers and coronary risk, these effects have tended to disappear after controlling for epigenetic and confounding factors and with increasing sample sizes. Finally, much attention is being devoted to non-invasive imaging of the coronary arteries. Such methods hold much promise as a screening test to exclude coronary stenosis in low-risk individuals. However, the measurement of calcium content of the arterial wall by EBCT has yet to prove its usefulness as a predictor of coronary events.
Nutr Metab Cardiovasc Dis 2000 Jun
PMID:Primary prevention of coronary heart disease: from controversy to consensus. 1100 23

Insulin resistance and hyperinsulinemia are the critical characteristics of the metabolic syndrome that is associated with abdominal obesity and are the early manifestations of its progression to type 2 diabetes. These metabolic abnormalities are becoming recognized as a major contributor to cardiovascular disease. The experimental studies required to elucidate the underlying mechanisms and to develop effective preventative strategies will require the use of appropriate animal models and these are available. The evidence from such research indicates that a wide range of interventions (including peroxisome proliferator activator receptor agonists, insulin-sensitizing agents, statins, fibrates, angiotensin-converting enzyme inhibitors, estrogen receptor modulators, lipid-based nutriceuticals, and ethanol) can markedly reduce or prevent vasculopathy and ischemic cardiac lesions in animal models. Overall, the results suggest that early damage to the vascular wall, both in function and presenting as atherosclerotic lesions, is secondary to long-term hyperinsulinemia and, especially, to postprandial peaks in plasma insulin levels, and is exacerbated by the accompanying hyperlipidemia. Effective treatment will, of necessity, be preventative and will necessitate diagnostic approaches that can identify asymptomatic individuals at high risk for vascular damage and eventual progression to type 2 diabetes. Therapeutic targets in this population include insulin sensitivity and the associated signal transduction pathways, the peroxisome proliferator activator receptor-alpha and -gamma systems, and the complex pathways leading from acetyl CoA and the citric acid cycle to the synthesis of fatty acid and the storage of triglyceride. These pharmacological approaches offer the prospect of preventing a significant proportion of cardiovascular disease.
Curr Drug Targets Cardiovasc Haematol Disord 2001 Dec
PMID:Reduction and prevention of the cardiovascular sequelae of the insulin resistance syndrome. 1276 60

The metabolic syndrome is a highly prevalent clinical entity. The recent Adult Treatment Panel (ATP III) guidelines have called specific attention to the importance of targeting the cardiovascular risk factors of the metabolic syndrome as a method of risk reduction therapy. The main factors characteristic of this syndrome are abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance (with or without glucose intolerance), prothrombotic and proinflammatory states. An insulin resistance following nuclear peroxisome proliferator activated receptors (PPAR) deactivation (mainly obesity-related) is the key phase of metabolic syndrome initiation. Afterwards, there are 2 principal pathways of metabolic syndrome development: 1) with preserved pancreatic beta cells function and insulin hypersecretion which can compensate for insulin resistance. This pathway leads mainly to the macrovascular complications of metabolic syndrome; 2) with massive damage of pancreatic beta cells leading to progressively decrease of insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. We suggest that a PPAR-based appraisal of metabolic syndrome and type 2 diabetes may improve our understanding of these diseases and set a basis for a comprehensive approach in their treatment.
Cardiovasc Diabetol 2003 Mar 23
PMID:Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). 1283 41

In many industrialized nations, obesity is now considered an epidemic, resulting in accelerated morbidity and mortality. Obesity is associated with an increased risk of coronary artery disease as well as the metabolic syndrome comprising abdominal obesity, increased fasting blood glucose levels, dyslipidemia and hypertension, which are all recognized cardiovascular risk factors. Diet, exercise, and lifestyle changes constitute important recommendations for treatment. Unfortunately, although effective in some individuals, these recommendations have proven to be ineffective in adequately addressing the broad, enlarging scope of this public health problem. Drug treatment is often indicated but is somewhat limited by the minimal number of well tolerated drugs that have proven to have long-term efficacy in maintaining bodyweight loss. For example, phentermine may result in modest bodyweight loss through suppression of appetite, but potential cardiovascular adverse effects exist and the efficacy is mainly short-term. Sibutramine, an inhibitor of serotonin and norepinephrine (noradrenaline) reuptake, may increase satiety and result in modest bodyweight loss. However, cardiovascular adverse effects may occur in susceptible patients. Nonetheless, sibutramine is one of the few drugs that has been approved by the US Food and Drug Administration (FDA) for bodyweight loss. Orlistat, a lipase inhibitor, is also approved by the FDA for bodyweight loss but may have bothersome gastrointestinal adverse effects, especially among patients who do not adhere to the recommended low-fat diet. Ongoing studies continue to evaluate other drug treatments that may result in bodyweight reduction through a number of different mechanisms. It is anticipated that the development of effective and well tolerated antiobesity drugs will elevate the pharmacologic treatment of obesity to the status of other cardiovascular risk factors and metabolic disorders. This may be especially important given that dyslipidemia, hypertension and type 2 diabetes mellitus are often secondary to, or exacerbated by, obesity.
Am J Cardiovasc Drugs 2002
PMID:Pharmacotherapy of obesity: currently marketed and upcoming agents. 1472 70

The metabolic syndrome is a compilation of factors characterized by insulin resistance and the identification of 3 of the 5 criteria of abdominal obesity, elevated triglycerides, decreased high-density lipoprotein (HDL) level, elevated blood pressure, and elevated fasting plasma glucose. According to census data from 2000, these criteria have lead to the diagnosis of approximately 47 million Americans with the metabolic syndrome, correlating with the 61% increase in the incidence of obesity between 1991 and 2000. Insulin resistance occurs when target tissues cannot respond properly to normal concentrations of insulin. The results are hypercoagulability, endothelial dysfunction, inflammation, and eventually coronary artery disease. Treatment involves lifestyle modification, including diet and exercise, to treat obesity and prevent the development of diabetes. Patients who meet the criteria for the metabolic syndrome may also be treated with insulin-sparing and insulin-sensitizing medications that help to improve endothelial function, vascular reactivity, and vascular inflammation. Ultimately, treatment goals are to prevent cardiovascular disease by both altering the risk factors that are components of the syndrome, and treating the lifestyle issues inherent to the disease process, such as caloric restriction and increased physical activity. There are 2 million more women than men in the United States categorized as being obese, with the trend of obesity and diabetes increasing. In the last decade there has been a 74% increase in obesity, mostly in women. This epidemic needs to be understood and managed to prevent further morbidity and mortality owing to diabetes and cardiovascular disease.
Prog Cardiovasc Dis
PMID:The metabolic syndrome: an emerging health epidemic in women. 1496 55

Increasing efforts are being made to address, in public health policy (PHP), both the persistence of nutritional deprivation in economically disadvantaged communities, and the increase in so-called "chronic disease" (abdominal obesity, diabetes, cardiovascular disease, certain cancers, osteoporosis, arthritides, and inflammatory disease) in communities at all stages of economic development. The problems in the "chronic disease" descriptor are that its origins may be as early as conception, rather than during the postnatal lifespan, or even in previous generations; it may appear abruptly or slowly; and it may be amenable to environmental and behavioural intervention well into its course and in older age groups. It is also not necessarily "non-communicable", a qualifier often used for "chronic disease" (chronic non-communicable disease or CNCD) and often has inflammatory features, for example the inflammatory marker C-reactive protein is a predictor of macrovascular disease and ischaemic events can, in part, be prevented in the affected by influenzal vaccination. The nexus between immunodeficiency, inflammatory processes and nutritional status which is characteristic of "infective" and food-borne illness, is also more and more evident in "chronic disease". It may be more helpful to consider "chronic disease" as "eco-disease" with its environmental and behavioural contributors, and to regard that which is clearly nutritionally dependent as "eco-nutritional disease".
Nutr Metab Cardiovasc Dis 2004 Feb
PMID:Nutrition and prevention of chronic diseases: a unifying eco-nutritional strategy. 1505 57

The metabolic syndrome is intended to identify patients who have increased risk of diabetes and/or a cardiac event due to the deleterious effects of weight gain, sedentary lifestyle, and/or an atherogenic diet. The National Cholesterol Education Program's Adult Treatment Panel III definition uses easily measured clinical findings of increased abdominal circumference, elevated triglycerides, low high-density lipoprotein-cholesterol, elevated fasting blood glucose and/or elevated blood pressure. Three of these five are required for diagnosis. The authors also note that other definitions of metabolic syndrome focus more on insulin resistance and its key role in this syndrome. This review focuses on how treatment might affect each of the five components. Abdominal obesity can be treated with a variety of lower calorie diets along with regular exercise. Indeed, all of the five components of the metabolic syndrome are improved by even modest amounts of weight loss achieved with diet and exercise. For those with impaired fasting glucose tolerance, there is good evidence that a high fiber, low saturated fat diet with increased daily exercise can reduce the incidence of diabetes by almost 60%. Of note, subjects who exercise the most, gain the most benefit. Metformin has also been shown to be helpful in these subjects. Thiazolidinedione drugs may prove useful, but further studies are needed. Although intensified therapeutic lifestyle change will help the abnormal lipid profile, some patients may require drug therapy. This review also discusses the use of statins, fibrates, and niacin. Likewise, while hypertension in the metabolic syndrome benefits from therapeutic lifestyle change, physicians should also consider angiotensin converting enzyme inhibitor drugs or angiotensin receptor blockers, due to their effects on preventing complications of diabetes, such as progression of diabetic nephropathy and due to their effects on regression of left ventricular hypertrophy. Aspirin should be considered in those with at least a 10% risk of a coronary event over 10 years. Finally, three related conditions, nonalcoholic fatty liver disease, polycystic ovary syndrome and protease inhibitor associated lipodystrophy improve with therapeutic lifestyle change. Although metformin is shown to be useful with polycystic ovary syndrome, the data supporting drug therapy for the other syndromes is less convincing. More robust studies are needed before any firm recommendations can be made.
Expert Rev Cardiovasc Ther 2004 Mar
PMID:Treatment of metabolic syndrome. 1515 70

Eighteen million Americans have type 2 Diabetes Mellitus (DM) while another 40 million have impaired glucose tolerance. Atherosclerotic heart disease is the leading cause of death in patients with diabetes mellitus. In addition to the increased risk for CardioVascular Disease (CVD), patients with diabetes have a worse prognosis than nondiabetics when they suffer an ischemic event. Insulin resistance is increasingly recognized as a chronic, low-level, inflammatory state. Hyperinsulinemia has been proposed as the forerunner of hypertension, low high-density lipoprotein cholesterolemia, hypertriglyceridemia, abdominal obesity, and altered glucose tolerance, linking all these abnormalities to the development of coronary vascular disease. Atherosclerosis and insulin resistance share similar pathophysiological mechanisms, due to the actions of proinflammatory cytokines. The dynamic inflammatory milieu found in diabetes explains the susceptibility of diabetics to CVD and the potential mechanism by which aspirin may prevent CVD in diabetics. Aspirin decreases the risk for CVD in diabetic patients by a variety of established and novel mechanisms. Therapeutic strategies that lesson the CVD risk in diabetic patients, including the use of aspirin for primary and secondary prevention, are potentially very important. This review article addresses the antiatherosclerotic effects of aspirin, the potential anti-diabetic effects of aspirin, and the clinical trial evidence for CVD prevention by aspirin in diabetics. We also present recommendations for the use of aspirin in the diabetic population and the current guidelines put forth by the American Heart Association and by the American Diabetes Association.
Cardiovasc Drug Rev 2004
PMID:Prevention of cardiovascular complications of diabetes mellitus by aspirin. 1549 69

The risk of developing cardiovascular disease has recently been associated with a set of metabolic and physiological risk factors that include abdominal obesity, atherogenic dyslipidemia, hypertension, and elevated plasma glucose. The term most commonly used to describe this conglomeration of risk factors is the metabolic syndrome. Coronary heart disease risk is tripled in those individuals with this syndrome. Primary treatment focuses on weight reduction and physical activity to reduce risk factors and prevent the progression to cardiovascular disease. This article will review the definition, prevalence, pathogenesis, and treatment of the metabolic syndrome in women and will discuss the role of polycystic ovarian syndrome in relation to the metabolic syndrome.
J Cardiovasc Nurs
PMID:The metabolic syndrome in women: a growing problem for cardiac risk. 1648 27

Metabolic syndrome affects approximately 44% of the US population over the age of 50 years. Although conflicting definitions exist, the syndrome is typically characterized by abdominal obesity, dyslipidemia, hypertension, and insulin resistance. Thus, it is a major risk factor for both coronary heart disease and type 2 diabetes. Furthermore, the risk of cardiovascular (CV) death is significantly increased in patients with diabetes and/or the metabolic syndrome. Although very few studies exist in patients with the metabolic syndrome, lifestyle changes and drug intervention targeted at the individual components have been shown to reduce the risk of developing diabetes and the incidence of CV disease in high-risk patients. Because many of the conventional antihypertensive drugs may affect the development of new onset diabetes, both positively and negatively, the choice of therapy is particularly important in this population. However, the long-term clinical trials to date have either not included new onset diabetes as a protocol end point or used various different criteria, making comparisons difficult. This review assesses the need for future research into metabolic syndrome and discusses whether clinical surrogates for CV end points, such as new onset diabetes, should be included in clinical trials of new drugs, new regimens, or new indications.
J Cardiovasc Pharmacol 2006 Mar
PMID:Metabolic syndrome, new onset diabetes, and new end points in cardiovascular trials. 1663 92


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