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

Healthy People 2000, the national strategy for improving the health of individuals in the United States, provides direction for the prevention of chronic illnesses, injuries, and infectious diseases by specifying desired outcomes for specific populations. The authors focus on outcomes for several illnesses and conditions known to significantly affect the health of women who are menopausal or postmenopausal. These include osteoporosis, hypertension, cardiovascular disease, stroke, diabetes mellitus type 2, congestive heart failure, and obesity. Suggestions for advanced nurse practitioner assessment and intervention are provided for the reader.
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PMID:Is anyone listening? Does anyone care? Menopausal and postmenopausal health risks, outcomes, and care. 1077 59

The obese ZDFxSHHF-fa/fa(cp) model was developed by crossing lean female Zucker Diabetic Fatty (ZDF +/fa) and lean male Spontaneously Hypertensive Heart Failure (SHHF/Mcc-fa(cp), +/fa) rats. The purpose of the present study was to determine renal function and morphology, hemodynamics, and metabolic status in ZDFxSHHF rats. Two sets of experiments were conducted. First, we evaluated heart and kidney function and metabolic status in aged (46 weeks old) male obese ZDFxSHHF and age matched obese SHHF rats, lean Spontaneously Hypertensive (SHR) and lean normotensive Wistar Kyoto (WKY) rats. In the second set of experiments, renal function and structure as well as metabolic and lipid status were determined in lean (LN) and obese (OB) adult (29-weeks of age) ZDFxSHHF rats. At 46 weeks of age ZDFxSHHF rats are hypertensive expressing marked cardiac hypertrophy associated with diastolic dysfunction and preserved contractile function. Fasted hyperglycemia and hyperinsulinemia are accompanied by moderate hypercholesterolemia and hypertriglyceridemia. Obese aged ZDFxSHHF have marked renal hypertrophy, a 3-8 fold decrease in creatinine clearance (compared with SHHF, SHR and WKY), a high percent of segmental + global glomerulosclerosis (59.8%+/-10.8), and severe tubulointerstitial and vascular changes. Obese ZDFxSHHF rats die at an early age (approximately 12 months) from end-stage renal failure. Studies conducted in 29-week animals showed that, although both LN and OB 29-week old animals are hypertensive, OB animals have more severely compromised renal function and structure as compared with lean litter-mates (kidney weight: 2.56+/-0.16 vs. 1.61+/-0.12 g; creatinine clearance: 0.42+/-0.04 vs. 1.24+/-0.13 L/g kid/day; renal vascular resistance 12.39+/-1.4 vs. 6.14+/-0.42 mmHg/mL/min/g kid; protein excretion: 556+/-16 vs. 159+/-9mg/day/g kid, p < 0.05, OB vs. LN, respectively). Obesity is also associated with hyperglycemia (424+/-37 vs. 115+/-11 mg/dL), hyperinsulinemia (117.2+/-8.8 vs. 42.3+/-3.5 microU/mL), hypertriglyceridemia (5200+/-702 vs. 194+/-23 mg/dL), hypercholesterolemia (632+/-39 vs. 109+/-4mg/dL), and presence of segmental + global glomerulosclerosis (20.1+/-3.2% vs. 0.1+/-0.1%) with prominent tubular and interstitial changes (p < 0.05, OB vs. LN, respectively). In summary, the present study indicates that the crossing of rat strains of nephropathy produces hybrids that carry a high risk for severe renal dysfunction. The ZDFxSHHF rats express insulin resistance, hypertension, dislipidemia and obesity and develop severe renal dysfunction. In addition, the hybrids do not develop some of the complications (hydronephrosis or congestive heart failure) common for the parental strains that may compromise studies of renal function and structure. Therefore, the ZDFxSHHF rat may be a useful model fore valuating risk factors and pharmacological interventions in chronic renal failure.
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PMID:Renal function and structure in diabetic, hypertensive, obese ZDFxSHHF-hybrid rats. 1090 Nov 78

Diabetic patients have a higher prevalence of hypertension, dyslipidemia and obesity. However, diabetes is by itself a major independent risk factor for cardiovascular disease. About two-thirds of total mortality are due to diabetic macroangiopathy. It is characterised by accelerated atherosclerosis, with more severe, more extensive and more diffuse lesions, as compared with nondiabetic patients. Patients with diabetes present more frequently acute pulmonary oedema despite similar infarct sizes than do nondiabetic patients. They are more frequently at risk for ventricular dysfunction, for ventricular aneurysm and for congestive heart failure. At the time of diagnosis of type 2 diabetes, more than 50% of patients have pre-existing coronary heart disease, probably related to painless ischemia, caused by an autonomic denervation of the heart in diabetic patients. International recommendations suggest that all diabetic patients should be evaluated at least annually for the development or progression of risk factors that would prompt cardiac testing. The standard bicycle exercise test should be chosen in an asymptomatic patient with only one other risk factor and with a normal resting ECG. For all other diabetic patients, stress echocardiography or stress myocardial perfusion imaging should be preferably chosen.
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PMID:[Cardiac complications of type 2 diabetes]. 1092 96

Longitudinal and cross-sectional studies suggest that a large number of obese patients have a high prevalence of hypertension. This association causes the following changes: insulin and leptin resistance with a suppressed biologic activity of natriuretic peptide, which contributes to sodium retention with concomitant expanded cardiopulmonary volume and increased cardiac output. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistance. These changes lead to structural adaptations in the heart characterized by concentric-eccentric left ventricular hypertrophy. The hypertrophic condition provides the basis for the development of congestive heart failure and cardiac arrhythmias that may explain the higher rates of cardiac sudden death in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitial hydrostatic pressure and tubular sodium reabsorption. The consequent increase in renal flow and glomerular filtration enhances albuminuria excretion and the susceptibility to the development of renal damage. In summary, the hemodynamic and structural adaptations related to obesity hypertension is the cause of greater risk for adverse cardiovascular and renal events.
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PMID:Obesity-hypertension: the effects on cardiovascular and renal systems. 1113 Jul 76

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.
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PMID:Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. 1130 64

Therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy consists of dietary salt restriction, inspired oxygen, diuretics, and angiotensin-converting enzyme inhibitors or, if left ventricular systolic dysfunction is present, hydralazine/isosorbide dinitrate. Digitalis may be indicated in selected cases. These measures may also be useful chronically in association with weight loss. Substantial weight loss is capable of reversing all of the hemodynamic abnormalities associated with obesity except elevation of left ventricular filling pressure. Substantial weight loss may also reduce left ventricular mass and improve left ventricular diastolic filling in those with left ventricular hypertrophy before weight loss. Left ventricular systolic function also improves after weight loss in those with impaired pre-weight-loss systolic function. These beneficial effects of weight loss occur partly because of favorable alterations in left ventricular loading conditions. Substantial weight loss in patients with congestive heart failure associated with obesity cardiomyopathy produces a reversal of many of the clinical manifestations of cardiac decompensation and improves New York Heart Association functional class in most patients.
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PMID:Management of obesity cardiomyopathy. 1130 65

Hypertension occurs more commonly in obese than in lean persons at virtually every age. A variety of endocrine, genetic, and metabolic mechanisms have been linked to the development of obesity hypertension. These include insulin resistance and hyperinsulinemia, increased serum aldosterone levels, salt sensitivity and expanded plasma volume in the presence of increased peripheral vascular resistance, a genetic predisposition, and possibly increased leptin levels. Pressure and volume overload are present in obese hypertensives. This leads to a mixed eccentric-concentric form of left ventricular hypertrophy and increases the predisposition to congestive heart failure. Weight loss, even in modest decrements, is effective in reducing obesity-hypertension, possibly by ameliorating several of the proposed pathophysiologic mechanisms. There are currently no specific recommendations concerning pharmacotherapy of obesity-hypertension because each drug group has pros and cons.
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PMID:Obesity, hypertension, and the heart. 1130 66

Left ventricular diastolic properties are important markers of pump function and are frequently abnormal when myocardial insults alter tissue structure. Alterations can be limited to the early diastolic phase (early active relaxation) or to late diastolic filling (late ventricular compliance), but more often involve regulation of both phases of diastole. In asymptomatic patients with arterial hypertension, left ventricular relaxation is often prolonged, independently, at least in part, of cardiac loading conditions and left ventricular geometry, but this abnormality is associated with early signs of systolic dysfunction. Uncontrolled hypertension, diabetes, and obesity are most often associated with ischemic heart disease and impaired diastolic function. Reducing blood pressure with antihypertension therapy will reduce myocardial afterload, regress LVH, and improve systolic and diastolic function. In patients with symptoms of CHF with a normal ejection fraction, however, changes in therapy may be indicated. Greater emphasis should be placed on using medications that decrease myocardial load, but also reduce the effects of neurohormonal activation. (c)2001 by Le Jacq Communications, Inc.
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PMID:Diastolic dysfunction in arterial hypertension. 1141 76

Obesity has been shown to be an independent risk factor for coronary heart disease. The insulin resistance associated with obesity contributes to the development of other cardiovascular risk factors, including dyslipidemia, hypertension, and type 2 diabetes. The coexistence of hypertension and diabetes increases the risk for macrovascular and microvascular complications, thus predisposing patients to cardiac death, congestive heart failure, coronary heart disease, cerebral and peripheral vascular diseases, nephropathy, and retinopathy. Body weight reduction increases insulin sensitivity and improves both blood glucose and blood pressure control. Metformin therapy also improves insulin sensitivity and has been associated with decreases in cardiovascular events in obese diabetic patients. Antihypertensive treatment in diabetics decreases cardiovascular mortality and slows the decline in glomerular function. However, pharmacological treatment should take into account the effects of the antihypertensive agents on insulin sensitivity and lipid profile. Diuretics and beta-blockers are reported to reduce insulin sensitivity and increase triglyceride levels, whereas calcium channel blockers are metabolically neutral and ACE inhibitors increase insulin sensitivity. For the high-risk hypertensive diabetic patients, ACE inhibition has proven to confer additional renal and vascular protection. Because hypertension and glycemic control are very important determinants of cardiovascular outcome in obese diabetic hypertensive patients, weight reduction, physical exercise, and a combination of antihypertensive and insulin sensitizers agents are strongly recommended to achieve target blood pressure and glucose levels.
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PMID:Treatment of obesity hypertension and diabetes syndrome. 1156 61

This article gives an overview, citing animal and clinical studies, of the effects of increased intra-abdominal pressure (IAP) in severe obesity. Animal studies demonstrate that increased IAP increases pleural pressure, cardiac filling pressures, femoral venous pressure, renal venous pressure, systemic blood pressure, and vascular resistance, renin and aldosterone levels, and intracranial pressure. Thus, the comorbidities presumed secondary to increased IAP in obese patients include congestive heart failure, hypoventilation, venous stasis ulcers, gastroesophageal reflux, urinary stress incontinence, incisional hernia, pseudotumor cerebri, proteinuria, and systemic hypertension.
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PMID:Effects of increased intra-abdominal pressure in severe obesity. 1158 45


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