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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with combined dyslipidemia are at high risk for coronary artery disease and often require combination drug therapy to achieve lipid levels recommended by the US National Cholesterol Education Program's third Adult Treatment Panel (ATP III). In addition to recommendations for low-density lipoprotein (LDL) cholesterol and triglyceride levels, ATP III established non-high-density lipoprotein (HDL) cholesterol goals for individuals with triglycerides >or=2.26 mmol/L (>or=200 mg/dL). It also introduced certain criteria for the diagnosis of the metabolic syndrome, a clustering of risk factors (abdominal obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure, impaired fasting glucose) that increases cardiovascular risk and is common in patients with combined dyslipidemia. Statin monotherapy has been shown to benefit these patients, and additional benefit may be obtained by combination therapy that provides greater reductions in both LDL cholesterol and triglycerides as well as greater increases in HDL cholesterol. However, combining a statin with either niacin or a fibrate may increase the risk for myopathy and therefore requires careful monitoring and evaluation of the risk-benefit ratio for each patient. Moreover, combination therapy may be associated with increased drug costs and decreased patient compliance. Recently developed agents that may improve the effectiveness of combination therapy include ezetimibe-a cholesterol absorption inhibitor-and a formulation that combines extended-release niacin and lovastatin in a single pill. Clinical trials are needed to determine the optimal treatment in patients with combined dyslipidemia.
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PMID:Combination therapy for combined dyslipidemia. 1246 37

Evolutionary pressures have probably amplified the mechanisms for minimizing the impact of environmental factors through compensatory maternal mechanisms. Nevertheless, experimentally there are clear long-term programming effects of manipulations to the maternal diet on the likelihood of neural-tube defects associated with folate deficiency The fat/lean ratios of the newborn, and subsequent development, seem to be linked to amino acid or folate supply. An altered balance in the hypothalamic-pituitary-adrenal axis, which experimentally has profound effects on brain development, is induced by low-protein maternal diets. Such diets are linked to a reduced pancreatic capacity for insulin production and to an altered hepatic architecture, with a change in the control of glucose metabolism. Human studies suggest that what happens in pregnancy is modified by the child's diet in the first months of life. Low birthweight is linked to early stunting, and predisposes to abdominal obesity and metabolic syndrome in later life. Metabolic syndrome amplifies the risks of diabetes, hypertension, coronary heart disease and probably some cancers. Mothers with gestational diabetes are themselves prone to early type 2 diabetes and produce heavier babies prone to childhood obesity and adolescent type 2 diabetes. There is increasing evidence of an intergenerational effect, with big babies being prone to excess weight gain, which then, in girls, predisposes them to diabetes in pregnancy, which, in turn, promotes an accelerating cycle of early diabetes in subsequent generations. Essential fatty acids and fat soluble vitamins are important, but we need early interventions and monitoring systems to justify coherent policies.
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PMID:Will feeding mothers prevent the Asian metabolic syndrome epidemic? 1249 42

Insulin resistant metabolic syndrome is a major clinical disorder including hyperlipidaemia, hypertension, impaired glucose tolerance and/or type 2 diabetes and central obesity, which are well established cardiovascular risk factors. We report the case of a 61-year-old woman who developed severe hypercholesterolaemia and hypertriglyceridaemia after liver transplantation. In her forties she had hypertension, mixed hyperlipidaemia, mild hyperglycaemia and moderate abdominal obesity, suggesting the presence of the metabolic syndrome. She had liver enzyme elevation and severe steatosis and hepatomegaly at ultrasonography. At age 52, cryptogenic liver cirrhosis was diagnosed and rapidly progressing liver failure developed. In 1992 she underwent liver transplantation. Seven years after transplant the patient had abdominal obesity, high blood pressure, marked hypercholesterolaemia, hypertriglyceridaemia and moderate elevation of alanine aminotransferase. She also had impaired glucose tolerance and markedly increased basal and post-glucose load plasma insulin levels. Steatohepatitis was demonstrated by serial liver biopsies. This is the first case that reports the recurrence of the metabolic syndrome following liver transplantation. We postulate that metabolic syndrome may have promoted fatty liver and subsequent progression to end stage liver disease. We also stress the need for careful management of the metabolic syndrome in order to decrease the long-term risk for cardiovascular disease.
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PMID:Recurrence of insulin resistant metabolic syndrome following liver transplantation. 1254 3

Metabolic syndrome, the clustering of hyperglycemia, hypertension and dyslipidemia, increases the risk of coronary heart disease. Abdominal obesity is an important cue for the clinician to consider metabolic syndrome. Measurement of waist circumference is a simple means of identifying abdominal obesity. The development and distribution of pocket tape measures to medical students, residents and attending physicians were initiated to enhance identification and treatment of metabolic syndrome. Distribution of the tape measures was added to a cardiovascular nutrition component in a 4th-y medical school curriculum. The nutrition component continued to include computer-based cases and pocket reference cards. Limited data suggest that the addition of pocket tape measures to the nutrition component of an ambulatory care clerkship may increase the percentage of medical students who use waist circumference to identify patients at risk for metabolic syndrome. It is anticipated that student use will increase with role modeling by residents and attending physicians.
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PMID:Pocket tape measure for waist circumference: training medical students and residents on a simple assessment of body composition. 1256

The aim of the present study was to investigate the association between the serum lipid profile and components of the metabolic syndrome, such as central obesity (anthropometric, computed tomography and fat cell data), insulin, sex-hormone-binding-globulin (SHBG) and different hormones influencing this important syndrome, e.g. sex steroids, leptin and tumor necrosis factor-alpha (TNF-alpha). The sample consisted of 85 obese patients (30 men and 55 women) who had undergone abdominal surgery. Fasting serum lipids were analysed, as well as anthropometric and computed tomography data, perivisceral and subcutaneous fat cell size and serum glucose and hormones. Abdominal fat revealed itself as an important correlator of the adverse changes in plasma lipoprotein levels, the waist-to-hip-ratio and waist-to-thigh-ratio being the best morphological correlators in men and women, respectively. Intra-abdominal fat (VA) correlated significantly and positively to perivisceral fat cell size in women, while no correlation was found between subcutaneous fat accumulation (SA) and adipocyte size in both genders. Perivisceral fat cell size showed the greatest number of correlations with the adverse plasma lipid profile compared to that in the subcutaneous depot. SHBG and sex steroids showed a negative correlation with serum lipids considered a cardiovascular risk. In contrast, TNF-alpha and C-peptide were inversely correlated with potential protector lipids. In conclusion, abdominal obesity, adipocyte hypertrophy from visceral fat, serum TNF-alpha and C-peptide seem to be the best correlators of the lipoprotein disturbance characteristic of the metabolic syndrome, whereas SHBG and sex steroids could play a protective role regarding the lipid profile associated to this syndrome.
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PMID:Interrelationship between serum lipid profile, serum hormones and other components of the metabolic syndrome. 1260 9

The prevalence of marked obesity is increasing rapidly among adults and has more than doubled in 10 years. Sixty-one percent of the adult population of the United States is overweight or obese. Americans are the fattest people on earth. Paradoxically these increases in the numbers of persons who are obese or overweight have occurred during recent years when Americans have been preoccupied with numerous dietary programs, diet products, weight control, health clubs, home exercise equipment, and physical fitness videos, each "guaranteed" to bring rapid results. Overweight and obesity are also world problems. The World Health Organization estimates that 1 billion people around the world are now overweight or obese. Westernization of diets has been part of the problem. Fruits, vegetables, and whole grains are being replaced by readily accessible foods high in saturated fat, sugar, and refined carbohydrates. Since class 3 obesity (morbid or extreme obesity) is associated with the most severe health complications, the incidence of hypertension, stroke, heart disease, diabetes, and peripheral vascular disease will increase substantially in the future. Recently, obesity alone has been implicated in the development of cardiac hypertrophy and CHF. The metabolic syndrome associated with abdominal obesity, which includes insulin resistance, dyslipidemia, and elevated CRP levels, identifies subjects who have an increase in cardiovascular morbidity and mortality. Twenty to 25% of the adult population in the United States have the metabolic syndrome, and in some older groups this prevalence approaches 50%. The prevalence of overweight children in the United States has also been increasing dramatically, especially among non-Hispanic blacks and Mexican-American adolescents. Overweight children usually become overweight adults. Atherosclerosis begins in childhood. The degree of atherosclerotic changes in children and young adults can be correlated with the presence of the same risk factors seen in adults. As health providers, our direction is obvious!
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PMID:Obesity and the metabolic syndrome. 1262 76

Microalbuminuria clusters with the metabolic syndrome, and both conditions predict cardiovascular disease mortality. The reported relationships of microalbuminuria with the individual components of the metabolic syndrome (i.e., hyperglycemia, insulin resistance, hypertension, dyslipidemia, abdominal obesity) are variable. Each of these components, as well as intrauterine effects and diet and other lifestyle factors, may contribute to elevated risk of microalbuminuria in certain population groups. Recent evidence indicates a role for oxidation and inflammation in cardiovascular disease, and endothelial dysfunction (exacerbated by factors such as dyslipidemia) may be the mediator of this relationship. Because endothelial dysfunction can also be manifested as microalbuminuria, this provides a potential explanation of the observed association of the metabolic syndrome, chronic inflammation, and microalbuminuria.
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PMID:Association of albuminuria and the metabolic syndrome. 1264 50

Abdominal obesity has been linked to the development of insulin resistance and Type 2 diabetes mellitus (DM2). By surgical removal of visceral fat (VF) in a variety of rodent models, we prevented insulin resistance and glucose intolerance, establishing a cause-effect relationship between VF and the metabolic syndrome. To characterize the biological differences between visceral and peripheral fat depots, we obtained perirenal visceral (VF) and subcutaneous (SC) fat from 5 young rats. We extracted mRNA from the fat tissue and performed gene array hybridization using Affymetrix technology with a platform containing 9 000 genes. Out of the 1 660 genes that were expressed in fat tissue, 297 (17.9 %) genes show a two-fold or higher difference in their expression between the two tissues. We present the 20 genes whose expression is higher in VF fat (by 3 - 7 fold) and the 20 genes whose expression is higher in SC fat (by 3 - 150 fold), many of which are predominantly involved in glucose homeostasis, insulin action, and lipid metabolism. We confirmed the findings of gene array expression and quantified the changes in expression in VF of genes involved in insulin resistance (PPARgamma leptin) and its syndrome (angiotensinogen and plasminogen activating inhibitor-1, PAI-1) by real-time PCR (qRT-PCR) technology. Finally, we demonstrated increased expression of resistin in VF by around 12-fold and adiponectin by around 4-fold, peptides that were not part of the gene expression platform. These results indicate that visceral fat and subcutaneous fat are biologically distinct.
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PMID:Differential gene expression between visceral and subcutaneous fat depots. 1266 Aug 71

The evidence for the adverse effects of obesity on women's health is overwhelming and indisputable. Obesity, especially abdominal obesity, is central to the metabolic syndrome and is strongly related to polycystic ovary syndrome (PCOS) in women. Obese women are particularly susceptible to diabetes, and diabetes, in turn, puts women at dramatically increased risk of cardiovascular disease (CVD). Obesity substantially increases the risk of several major cancers in women, especially postmenopausal breast cancer and endometrial cancer. Overweight and obesity are associated with elevated mortality from all causes in both men and women, and the risk of death rises with increasing weight. Curbing the twin epidemics of obesity and diabetes calls for not only changes in diet and lifestyle at individual levels but also changes in policy, physical and social environment, and cultural norms.
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PMID:Overweight and obesity in women: health risks and consequences. 1273 15

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.
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PMID:Reduction and prevention of the cardiovascular sequelae of the insulin resistance syndrome. 1276 60


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