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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A positive association exists between insulin resistance, dyslipidemia, and hypertension, specifically salt-sensitive hypertension. A subgroup of salt-sensitive normal and high renin hypertensives called nonmodulators (NM) manifest an inability to modulate the adrenal and renal blood flow responses to a change in dietary sodium. Therefore, we tested the hypothesis that the NM subgroup would be insulin resistant and dyslipidemic when compared with normal and high renin hypertensives, in whom modulation is intact (M). Forty-six nondiabetic hypertensive individuals were evaluated and their modulation status defined by either renal or adrenal criteria. Fasting blood was drawn for measurement of several metabolic factors. Since the NM group had a greater body mass index (BMI) it was subdivided into a "lean" subgroup that matched the BMI of the M group. The fasting insulin levels in both the total NM and lean NM groups was significantly higher than in the M group (P = .013 and .04, respectively). There were no differences in age, blood pressure, or plasma/serum levels of glucose, triglycerides, total cholesterol, or potassium. NM had elevated fasting insulin levels compared to M, compatible with an insulin resistant state, but this insulin resistance are dissociable in the hypertensive population.
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PMID:Metabolic derangements in nonmodulating hypertension. 854 Oct 1

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.
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PMID:Insulin resistance and hyperinsulinemia in hypertension. 857 90

Obesity is associated with risk-factor clustering, including risk factors for hypertension, hyperinsulinemia, resistance to insulin's lowering of glucose and fatty acid concentrations, and a complex dyslipidemia. Obese hypertensive subjects are presumed to be salt sensitive because of the antinatriuretic actions of insulin. However, in our studies obese hypertensive subjects aged < 45 y were not more salt sensitive than were lean individuals. Subjects with the greatest evidence for risk-factor clustering had higher renin and aldosterone concentrations, which increased with salt restriction. The greater rise of fatty acids and activation of the renin-angiotensin system may explain the larger elevations of blood pressure, insulin, and triacylglycerol with salt restriction in high-risk subjects than in low-risk subjects. Regardless of mechanism, the adverse effects of short-term, very-low-salt diets in high-risk subjects suggest that continued moderation in advice for universal salt restriction is appropriate.
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PMID:Adverse effects of short-term, very-low-salt diets in subjects with risk-factor clustering. 902 63

Cardiomyopathy in chronic uremia results from pressure and volume overload. The former causes concentric left ventricular [LV] hypertrophy, results from hypertension and aortic stenosis, and is also associated with diabetes mellitus and anemia. Volume overload causes LV dilatation, results from arteriovenous shunting, salt and water overload, and anemia, and is also associated with ischemic heart disease, hypertension, and hypoalbuminemia. Decreased major arterial compliance and an early return of arterial wave reflections are also associated with the extent of LV hypertrophy. Cardiomyopathy predisposes to diastolic and systolic dysfunction. The latter results from myocyte death, and predisposing factors include ischemic heart disease and the uremic environment. Ischemic heart disease may be atherosclerotic or nonatherosclerotic in origin. Multiple factors contribute to the vascular pathology of chronic uremia, including injury to the vessel wall, dyslipidemia, prothrombotic factors, increased oxidant stress, and hyperhomocysteinemia. Ischemic risk factors include hypertension, LV hypertrophy, hypoalbuminemia, and perhaps hyperparathyroidism. The clinical consequences of cardiomyopathy include heart failure, ischemic heart disease, dialysis hypotension, and arrhythmias. The adverse impact of ischemic heart disease is probably mediated through the development of cardiac failure.
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PMID:Cardiac disease in chronic uremia: pathogenesis. 923 25

To investigate whether molecular variation in the renin gene contributes to the greater blood pressure of spontaneously hypertensive rats (SHR) versus normotensive Brown Norway (BN) rats, we measured blood pressure in an SHR progenitor strain and an SHR congenic strain that are genetically identical except at the renin gene and an associated segment of chromosome 13 transferred from the BN strain. Backcross breeding and molecular selection at the renin locus were used to create the SHR congenic strain (designated SHR.BN-Ren) that carries the renin gene transferred from the normotensive BN strain. We found that transfer of the renin gene from the BN strain onto the genetic background of the SHR did not decrease blood pressure in rats fed either a normal or high-salt diet. In fact, the systolic blood pressures of the SHR congenic rats tended to be slightly greater than the systolic blood pressures of the SHR progenitor rats. However, the congenic strain exhibited lower serum high-density lipoprotein cholesterol, and greater levels of total cholesterol, very-low-density lipoprotein, and intermediate-density lipoprotein cholesterol during administration of a high-fat, high-cholesterol diet. These findings demonstrate that (1) under the environmental circumstances of the current study, the greater blood pressure of SHR versus BN rats cannot be explained by strain differences in the renin gene and (2) a quantitative trait locus affecting lipid metabolism exists on chromosome 13 within the transferred chromosome segment. The SHR.BN-Ren congenic strain may provide a useful new animal model for studying the interaction between high blood pressure and dyslipidemia in cardiovascular disease.
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PMID:Effect of renin gene transfer on blood pressure in the spontaneously hypertensive rat. 945 31

Concomitant arterial hypertension and metabolic disorders is a frequent finding raising the risk of micro- and macrovascular complications. While prevalence of stroke and myocardial infarction is going down in hypertensives, end-stage renal disease (ESRD) becomes a bigger problem especially in diabetic hypertensives. The metabolic abnormalities are linked to the hypertension by the sympathoadrenal system mediated by insulin resistance (IR); subjects with hyperinsulinemia and increased sympathetic activity tend to have higher blood pressure, typical dyslipidemia, reduced fibrinolytic activity and other risk factors (RF) called metabolic syndrome of IR. Albuminuria (AUR) is considered as an important RF for the development of nephropathy, ESRD, cardiovascular diseases. AUR is a marker of cardiovascular and total mortality in diabetic and/or non-diabetic hypertensives. AUR reflects the endothelial dysfunction not only in glomerulus but also in the other arteries. Tissue Renin-Angiotensin System plays a significant role in the pathogenesis of hypertension and metabolic disorders; it affects the arterial wall, kidneys and heart longitudinally. Life style is very essential in the treatment of hypertension and metabolic disorders: rational diet with reduced amount of salt and animal proteins, non-smoking and sufficient physical activity. Antihypertensive drugs without any metabolic side effects and with the renal protection are necessary for the patients with hypertension and metabolic disturbances. ACE-inhibitors and/or some of the Ca-antagonists seems to be valuable especially as combined therapy.
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PMID:[New approaches in the treatment of hypertension in metabolic diseases]. 972 74

Non-immune mechanisms appear to be important in the majority of patients with lupus nephritis and progressive renal injury. Proteinuria, hypertension and dyslipidemia are associated non-immune risk factors often implicated in the deterioration of kidney function. There is ample animal experimental evidence that they are independent risk factors for progressive renal injury and their treatment results in amelioration of renal function. Proteinuria and hypertension, unlike dyslipidemia, have been shown to be independent risk factors for progressive renal injury in patients with lupus nephritis. Treatment of hypertension and proteinuria in the diabetic and non-diabetic progressive renal disease population results in stabilization of kidney function. Response to treatment should target both blood pressure of 120/80 and significant reductions in protein excretion. If protein excretion rate is unaltered by use of an angiotensin-converting enzyme inhibitor and salt restriction, one might resort to the use of an angiotensin II antagonist. Treatment of the dyslipidemia following good control of proteinuria, blood pressure and dietary change may not alter renal progression but should provide similar protection from accelerated vascular disease to the non-renal dyslipidemia population.
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PMID:Management of chronic renal insufficiency in lupus nephritis: role of proteinuria, hypertension and dyslipidemia in the progression of renal disease. 988 5

The enterohepatic circulation of bile salts and cholesterol plays a central role in maintaining whole body cholesterol homeostasis. Hepatic lipoprotein metabolism is reviewed and the role of disturbances in bile salt metabolism in the pathogenesis of dyslipidemias is discussed. Further, the manipulation of bile salt metabolism to treat dyslipidemia is reviewed.
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PMID:Role of the enterohepatic circulation of bile salts in lipoprotein metabolism. 1019 86

The most rapidly growing segment of the United States population is the geriatric group, especially those above 75 years of age. Hypertension, diabetes mellitus, and dyslipidemia increase with advancing years in Westernized, industrialized societies such as the United States. These disorders contribute significantly to strokes and myocardial infarctions and associated morbidity and mortality in our elderly population. The increase in these chronic disease processes with aging is related, in part, to increasing obesity, reductions in physical activity, and medications that predispose to these conditions (ie, nonsteroidal inflammatory agents and hypertension). Hypertension in the elderly is characterized by high peripheral vascular resistance/reduced cardiac output, impaired baroflex sensitivity, relatively greater systolic pressures, increased blood pressure variability, and a propensity to salt sensitivity. Type 2 diabetes in the elderly is related to alterations in body composition (ie, increased central adiposity and decreased lean body mass) and to reduced physical activity. There is an increasing body of evidence that aggressive treatment of hypertension and dyslipidemia in the elderly results in comparable, if not greater, reductions in cardiovascular morbidity and mortality in the elderly as in younger counterparts.
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PMID:Hypertension, hormones, and aging. 1081 Oct 49

In the insulin resistance (IR) syndrome, sex-specific differences have been reported. First, hypertension more often correlates with hyperinsulinemia in women than in men with the IR syndrome. In addition, salt sensitivity of blood pressure appears to be independent of the activity of the renin-angiotensin system in women, whereas in men there is a strong correlation between the two variables. Secondly, the dyslipidemia found in women with the IR syndrome is characterized by less postprandial plasma insulin, triglycerides, and fatty acid response to a standardized meal. However, this sex difference in lipids disappears after correction for visceral fat mass. Fat physiology and biochemistry differ between the two sexes. In women, adipose cells express less glucocorticoid receptors and less 11beta-hydroxysteroid dehydrogenase. In women visceral fat accumulation appears to be a constant feature of the IR syndrome but in men the syndrome can be present without central obesity. Lastly, during the reproductive years of women, the IR syndrome, such as in pre-eclampsia, may cause fetal growth retardation that has been proposed together with maternal malnutrition to be at the origin of the increased risk for impaired glucose tolerance, hyperinsulinemia, and hypertension in adult life. This gives yet another dimension to this disease in women since in essence they may ultimately transmit this syndrome to both sexes.
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PMID:Sex-related differences in the insulin resistance syndrome. 1127 93


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