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

Essential hypertension is frequently associated with several metabolic abnormalities, of which obesity, glucose intolerance, and dyslipidemia are the most common. This report discusses the epidemiologic evidence for the coexistence of these risk factors and questions why hyperinsulinemia and essential hypertension cosegregate. The euglycemic insulin clamp and the insulin suppression test are documented with respect to the physiologic functions of insulin, and the mechanisms of insulin resistance in essential hypertension are discussed. Evidence to suggest that insulin resistance is a marker for an "atherogenic syndrome" is reviewed. It is concluded that all the hemodynamic and metabolic disorders of essential hypertension and insulin resistance are closely related. The clinical approach to the patient with any of the abnormalities in question should take into consideration the whole cluster, with therapy aimed at ameliorating the entire hemodynamic-metabolic profile.
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PMID:Essential hypertension, metabolic disorders, and insulin resistance. 200 56

Effective blood pressure control with traditional high-dose diuretic therapy has led to a distinct decrease in cerebrovascular morbidity and mortality, but failed to achieve a satisfactory reduction of coronary complications and sudden death. The same applies also for beta blockers, although they have been shown to be effective in secondary prevention of myocardial infarction. It is suspected that conventional antihypertensive treatment has an unfavorable effect on coronary risk factors other than hypertension. For instance, thiazide-type diuretics can impair glucose tolerance and increase the potentially atherogenic serum low-density lipoprotein (LDL) cholesterol fraction and triglycerides. Beta blockers without partial intrinsic sympathomimetic activity increase serum triglycerides and tend to lower the potentially antiatherogenic high-density lipoprotein (HDL) cholesterol. Certain beta blockers may also impair glucose tolerance, particularly when they are combined with diuretics. Calcium channel blockers, angiotensin converting-enzyme inhibitors and alpha 1-receptor blockers do not adversely affect lipoprotein or carbohydrate profiles. The latter two drug classes may even increase insulin sensitivity, and alpha 1 blockers may also slightly improve lipid metabolism. The prognostic relevance of drug-induced dyslipidemia and/or glucose intolerance awaits further clarification. In the meantime, it is of clinical interest that several of the generally available antihypertensive drugs seem to be metabolically neutral or sometimes perhaps even potentially beneficial with regard to the lipoprotein and carbohydrate metabolism.
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PMID:Antihypertensive agents, serum lipoproteins and glucose metabolism. 202 Nov 13

The chronic hyperglycemia of non-insulin-dependent diabetes mellitus (NIDDM) evolves gradually and is usually preceded by more transient hyperglycemia, classified as impaired glucose tolerance (IGT). Already in this phase, there is an increased risk of cardiovascular complications, and many IGT subjects, like NIDDM patients, often display several of the metabolic and circulatory disturbances that are associated with hyperglycemia, e.g., insulin resistance, hyperinsulinemia and/or hyperproinsulinemia, delayed insulin release, dyslipidemia, and hypertension. Therefore, and because untreated hyperglycemia is a self-perpetuating condition, early detection and early intervention may be necessary to prevent the progression and complications of NIDDM. This in turn would necessitate screening procedures, and the therapeutic goal should include both euglycemia and normalization of plasma insulin, plasma lipids, and blood pressure. A study in the German Democratic Republic indicated that the mortality in screening-detected NIDDM patients did not differ from that in patients detected in routine care. In a Swedish study on screening-detected NIDDM subjects, only those who had IGT rather than manifest NIDDM could maintain fasting blood glucose less than or equal to 6 mM for 5 yr by hypocaloric dietary regulation alone. In those with screening-detected NIDDM, the delayed acute insulin release and net postprandial hyperglycemia were improved by addition of glipizide, and most managed to attain and maintain fasting blood glucose less than or equal to 6 mM for approximately 2 yr after such addition. However, after 4 yr, there was an increase in blood glucose, suggesting that preventive intervention either may not be possible or may have to start in the IGT phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Will sulfonylurea treatment of impaired glucose tolerance delay development and complications of NIDDM? 220 45

Genetic factors play an important role in the development of many common diseases of adulthood that result in early morbidity and mortality. Prevention of these disorders and their sequelae is best established through early detection and early intervention. Although it may be feasible to screen the entire population for some disorders (e.g., hypertension), this approach would be expensive and impractical for others (e.g., colon cancer). The family history provides an inexpensive and convenient method of identifying families at risk for premature diseases of adulthood. Family screening for a disorder should be recommended if there is increased risk for the disorder among family members, if screening methods are available to detect the condition at an early age or preclinical stage, and if early intervention will alter the course of the disease. For many disorders screening and intervention can prevent the occurrence of clinical disease. The prenatal counseling session affords an ideal setting for identifying families at risk for diseases of adulthood with major genetic components. By reviewing the family history, key family members can be identified and investigated, in order to establish a specific genetic diagnosis. At-risk relatives can then be counseled and screened for the disorder preclinically and premorbidly. The screening and intervention available for a disease depends on the nature of the disorder, our understanding of its physiology and etiology, and our current technology. The disorders discussed earlier are typical of conditions of adulthood that are influenced strongly by genetic factors, especially when they appear in younger adults. Atherosclerosis, colon cancer, and diabetes are complex phenotypes. Each can be caused by single-gene defects, but commonly the genetics are more complex. Empiric data help to establish the risk to an individual in the latter cases. In all three examples, early detection should lead to treatment, which can prevent more serious sequelae: by treating the dyslipidemia, coronary artery disease can be prevented; by removing the benign polyp, malignant cancer can be avoided; and when impaired glucose tolerance is detected, diet and exercise can prevent or delay frank diabetes and its complications. The complete evaluation of individuals at risk for disorders such as those in Table 1 and their families can be a complicated task. Referral to a center experienced in the genetics of common diseases often may be necessary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetics of common diseases of adulthood. Implications for prenatal counseling and diagnosis. 228 33

Cardiovascular disease, so common in the elderly, has become an urgent public health concern. Major contributing factors include hypertension, dyslipidemia, impaired glucose tolerance, physical indolence, and cigarette smoking. Diet plays a major role in atherogenesis by its influence in blood lipids, blood pressure, and glucose tolerance, although its impact in the elderly is speculative owing to a paucity of direct evidence. But a rationale exists. Most cardiovascular risk factors are more prevalent in the elderly than in the young adult. The rise in blood pressure and blood lipids with advancing age is not inevitable. Diet may contribute to hypertension through an excess of calories, saturated fat, cholesterol, or salt and a deficiency of potassium, calcium, and magnesium. Antiatherogenic diets low in saturated fat and cholesterol, rich in fiber, and with substitution of polyunsaturated fat and restricted calories tend to normalize serum lipids and to cause lesions to involute. Emphasis on vegetable protein and fiber-rich food has merit because they provide more fiber, polyunsaturated fatty acids, magnesium, selenium, complex carbohydrate, potassium, and copper, and less cholesterol, saturated fat, and sodium. The recommended fat-modified diets are adequate in protein, vitamins, and minerals and need not be deficient in any nutrient or economically nonfeasible. The accelerating decline in cardiovascular mortality, which has included the elderly, indicates that such disease is controllable and not inevitable, even in the elderly. The decrease has occurred concurrently with reduced consumption of saturated fat and cholesterol, increased use of vegetable oils, and improved levels of cardiovascular risk factors.
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PMID:Nutritional contributors to cardiovascular disease in the elderly. 351 Feb 41

Cigarette smoking has been associated with increased upper body fat deposition, as estimated by the waist to hip ratio, which has been shown to be associated with glucose intolerance and dyslipidemia in nonsmoking subjects. Whether smoking is at the origin of central adiposity and its related metabolic disturbances is unclear. Moreover, it is controversial whether smoking influences fuel metabolism. Therefore, young healthy male volunteers smoking more than 10 cigarettes/day for more than 5 yr (n = 14) were compared with nonsmokers (n = 13) matched for age, sex, body mass index, alcohol consumption, physical activity, as well as family history for hypertension, diabetes, obesity, and coronary heart disease. After an overnight fast, blood was drawn for chemistry, body composition was assessed by dual energy x-ray absorptiometry, and fuel metabolism was determined by indirect calorimetry. Nicotine uptake was estimated by 24-h urinary excretion of cotinine. Lean and fat body mass as well as their respective segmental distribution (i.e. arms, trunk, legs, and head), total bone mineral content, resting energy expenditure, and fat, carbohydrate, and protein oxidation were similar between smokers and nonsmokers. In contrast, 24-h urinary cotinine excretion (72.0 +/- 11.4 vs. 0.8 +/- 0.2 mumol/L.24 h; P < 0.001), plasma glucose (4.62 +/- 0.09 vs. 4.25 +/- 0.1 mmol/L; P < 0.01), total cholesterol (4.87 +/- 0.15 vs. 4.27 +/- 0.16 mmol/L; P < 0.02), low density lipoprotein cholesterol (3.05 +/- 0.19 vs. 2.43 +/- 0.16 mmol/L; P < 0.02), and apolipoprotein B concentrations (1.09 +/- 0.11 vs. 0.83 +/- 0.03 mmol/L; P < 0.03) were all higher in smokers than in nonsmokers. In smokers, 24-h urinary cotinine excretion positively correlated with the waist to hip ratio (r = 0.58; P = 0.03) and negatively with hip circumference (r = 0.87; P < 0.001). Moreover, 24-h cotinine excretion positively correlated with fat oxidation (r = 0.57; P = 0.03), but was independent of the other metabolic parameters studied. These results suggest that the dyslipidemia and glucose intolerance observed in smokers are not related to either central obesity or the amount of nicotine inhaled, but, rather, are due to some other component in cigarette smoke. In contrast, in smokers, fat oxidation increases with increasing nicotine uptake, a fact that might account for the often observed weight gain after cessation of smoking, thus suggesting different mechanisms of action of tobacco consumption on cholesterol and glucose metabolism on one side and fat oxidation on the other.
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PMID:Impact of chronic cigarette smoking on body composition and fuel metabolism. 760 76

Unlike classical microvascular complications, large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions have common genetic and environmental antecedents, i.e., they spring from a "common soil." It is now known that adverse environmental conditions, perhaps related to less-than-optimal nutrition, in fetal and early life are associated with an enhanced risk of both diabetes and cardiovascular disease many decades later. These same adverse environmental conditions are also associated with the development in adult life of abdominal obesity and the insulin-resistance syndrome (IRS). The IRS consists of glucose intolerance, hyperinsulinemia, dyslipidemia (high triglyceride and low high-density lipoprotein [HDL] cholesterol levels), and hypertension. Although the mechanism underlying this cluster is controversial, the statistical association is well established. All of the elements of the IRS have been documented as risk factors for type II diabetes. Some, but not all, of these elements are also cardiovascular disease risk factors, in particular, hypertension and low HDL cholesterol. Other factors associated with the IRS that may enhance cardiovascular disease risk are plasminogen activator inhibitor 1 and small, dense low-density lipoprotein particles. Whether insulin itself is a risk factor remains controversial, but recent epidemiological evidence has been mostly negative. This question has marked clinical relevance because if the IRS enhances cardiovascular disease risk by virtue of its concomitant factors and not the hyperinsulinemia per se, this would tend to alleviate concerns that intensive insulin management of type II diabetic subjects could enhance the risk of large-vessel atherosclerosis. Clinical trials are urgently needed to settle this point.
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PMID:Diabetes and cardiovascular disease. The "common soil" hypothesis. 769 2

Insulin resistance and reactive hyperinsulinemia occur not only in patients with obesity, impaired glucose tolerance or non-insulin-dependent (Type 2) diabetes mellitus, but also in many non-obese, non-diabetic individuals with essentiell hypertension and their normotensive, lean young offsprings. The common coexistance of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent occurrence of hypertension as well as dyslipidemia, obesity and diabetes Type 2 in a given individual. In the pathogenesis of hypertension, inappropriate vasoconstriction and/or a structural vasculopathy appears to be an important and ultimate causative event. Several pressor mechanisms are discussed and a distinct sodium retention appears to be almost obligatory associated with diabetes mellitus, while essential and particularly obesity-associated hypertension involves predominantly a tendency for sympathetic activation. Acute hyperinsulinemia on one hand causes arterial vasodilation and on the other hand enhances renal sodium reabsorption and sympathetic activity. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis. Insulin resistance affecting certain transmembrane cation transporters might lead to an elevation of intracellular cytosolic calcium levels thereby inducing inappropriate vasoconstriction. Nevertheless, whether insulin resistance and hyperinsulinemia contribute to the pathogenesis of hypertension per se is still unproven. Considering antihypertensive drugs, thiazide diuretics given in medium or high dosage as well as beta-blockers appear to promote insulin resistance, reactive hyperinsulinemia and dyslipidemia. Almost all calcium antagonists and the conventional sympthatolytics are metabolically neutral, while ACE-inhibitors and alpha 1-blockers tend to improve insulin resistance. In Type 2 diabetic patients, ACE-inhibitors exert in addition to their antihypertensive a potentially useful anti-diabetic effect. Nevertheless, the prognostic relevance of the metabolic side effects of antihypertensive drugs awaits further clarification.
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PMID:[Insulin resistance and arterial hypertension]. 771 73

Insulin resistance with consecutive hyperinsulinemia is associated with dyslipidemia in individuals with metabolic syndrome or "syndrome x". This dyslipidemia is characterized by a hypertriglyceridemia and reduced levels of HDL-(high density lipoprotein)cholesterol in plasma. Table 1 summarizes the alterations of lipoproteins in insulin resistance. In severe forms of insulin resistance LDL-(low density lipoprotein)cholesterol can be elevated as well. The hypertriglyceridemia is caused by an elevated synthesis and secretion of VLDL (very low density lipoprotein) in the liver and by reduced metabolism, mediated e.g. by lipoprotein lipase. The alterations of VLDL-metabolism are associated with a reduced concentration of HDL-cholesterol. In addition the composition of lipoprotein particles can be altered, which might interfere with their normal metabolism. Furthermore addition direct effects of insulin on cellular cholesterol metabolism have been described. These alterations in lipid metabolism which are due to an insulin resistance and hyperinsulinemia might be related to the increased coronary risk which has been observed in patients with metabolic syndrome. Therefore the diagnostic approach in patients with hypertriglyceridemia should consider the possibility of an underlying glucose intolerance or Type 2 diabetes. Therapeutic aims and strategies are discussed. In accordance to guidelines of the American Heart Association the goals of lipid-lowering therapy take into account the prevalence of various cardiovascular risk factors in an individual patient (Table 2). Principle actions of lipid-lowering drugs on plasma lipids are outlined in Table 3. Table 4 summarizes the effect of antihypertensive drugs on plasma lipids and lipoproteins, which should be considered in the treatment of patients with dyslipidemia.
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PMID:[Disorders of lipid metabolism in insulin resistance]. 771 75

The primary aim of the management of hypertension should be to prevent coronary heart disease. Antihypertensive treatment should have a beneficial effect on the risk factors associated with coronary heart disease, particularly hypertension, dyslipidemia, hyperinsulinemia, and/or glucose intolerance. Other important risk factors include central obesity, left ventricular hypertrophy, hypokalemia, and smoking. In patients genetically predisposed to essential hypertension, metabolic alterations characterized by insulin resistance, hyperinsulinemia, and dyslipidemia tend to occur already before the development of hypertension, obesity, or redistribution of body fat. In the treatment of normotensive or borderline hypertensive diabetic patients, angiotensin-converting enzyme (ACE) inhibitors have shown superiority to other agents due to their antiproteinuric effect and their beneficial influence on the glomerular filtration rate. ACE inhibitor treatment of patients with overt diabetic nephropathy has been reported to reduce the risk of mortality and the need for dialysis or transplantation. Beta blockers and thiazide diuretics are still the 'gold standard' of antihypertensive therapy in non-diabetic patients, as they offer at least some prognostic benefit, while the influence of the newer antihypertensive drugs on morbidity and mortality in these patients is not yet known. Nevertheless, since practicing physicians have to treat patients rather than statistical numbers, the current trend towards a more individualized selection, including the newer antihypertensive drugs with consideration of their metabolic, cardiac, and renal action profile, is also difficult to rebut. ACE inhibitors and most calcium antagonists have already evolved as the preferred drugs for the treatment of hypertension in diabetics due to their favorable effects on some of the cardiovascular and renal risk factors.
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PMID:Differential effects of antihypertensive drugs on hypertension: associated risk factors. 774 40


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