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Query: UMLS:C0242339 (dyslipidemia)
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During the last twenty years we witnessed a remarkable increase in knowledge of the mechanism as regards insulin action, the central hormone of metabolic regulations. Interest in cellular and molecular mechanisms of action was conditioned by a high prevalence of insulin resistance and the fact that insulin resistance holds a key position in the pathogenesis of many diseases, in particular atherosclerosis, obesity, hypertension, diabetes mellitus type II, ovarian hyperandrogenism and others. The syndrome of hyperinsulinaemia/insulin resistance is the basic component of the so-called X syndrome defined in 1988 by Reaven. It is encountered in subjects with a normal glucose tolerance but a predisposition for diabetes type II. If this disposition, probably genetic by nature, is potentiated by the central type of obesity and a sedentary lifestyle it can influence the development of hypertension and dyslipidemia. The sum of these factors promotes acceleration of atherosclerosis and frequently its premature manifestations: myocardial infarction and other cardiovascular diseases which hold the first place as regards causes of death on a world wide scale. It is important to identify but also to treat this complex not only metabolic risk factors for macrovascular diseases. It is a paradox that some drugs used as antihypertensives can cause deterioration of insulin resistance, subsequently influence in an adverse manner dyslipidemia and thus increase the metabolic risk of cardiovascular diseases. In the submitted paper the authors tried to summarize hitherto expressed views on the syndrome of hyperinsulinaemia and insulin resistance, using as a basic the results of their own work.
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PMID:[Hyperinsulinemia--the common denominator in type II diabetes mellitus,obesity, hypertension, hypertriglyceridemia and atherosclerosis]. 813 Nov 78

Several studies have indicated that insulin resistance, elevated blood pressure (BP), and dyslipidemia precede the onset of non-insulin-dependent diabetes mellitus (NIDDM). Little data, however, exist on the presence of renal disease in prediabetic subjects. We measured albumin excretion in a cross-sectional population study in subjects 65-74 years of age living in eastern Finland in relation to the risk of developing diabetes 3.5 years later. The prevalence of microalbuminuria (urinary albumin-to-urinary creatinine ratio > or = 2 mg/mmol) was 1.3-, 1.8-, and 2.0-fold higher among subjects with impaired glucose tolerance (n = 242), newly diagnosed NIDDM subjects (n = 92), and previously diagnosed NIDDM subjects (n = 136), respectively, compared with subjects with normal glucose tolerance (n = 826). Nondiabetic subjects with microalbuminuria had multiple abnormalities in cardiovascular risk factors including elevated BP, high triglyceride concentration, high insulin concentration, and a low high-density lipoprotein cholesterol concentration, a cluster of risk factors typical for prediabetic individuals. The relationship between microalbuminuria and the incidence of NIDDM over the 3.5-year follow-up was studied in 891 subjects who were free of diabetes at baseline. Converters to diabetes (n = 69) had a higher prevalence of hypertension (68.1 vs. 54.4%, P < 0.05) and a higher prevalence of microalbuminuria (43.5 vs. 30.4%, P < 0.05) than nonconverters (n = 822). In logistic regression analysis, microalbuminuria predicted the development of NIDDM independently of BP level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microalbuminuria precedes the development of NIDDM. 813 60

Association between insulin resistance and hypertension: 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 and 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 as well as dyslipidemia, obesity and type 2 diabetes in a given subject. Pathogenetic mechanisms: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to dysbalance of vasoactive substances and/or raised cytosolic Ca2+) and/or a structural vasculopathy is a very important ultimate causative event. In the presumed mosaic of participating pressor mechanisms, distinct Na+ retention is almost obligatory with diabetes mellitus, while essential and particularly obesity-associated hypertension probably involves a tendency for sympathetic activation. Development of insulin resistance: Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or being overweight. Acute hyperinsulinemia on the 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, and it has been proposed that insulin resistance in certain transmembranous cation exchange systems may elevate cytosolic Ca2+. Nevertheless, whether insulin resistance and/or hyperinsulinemia itself contribute to the pathogenesis of hypertension is still unclear.
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PMID:Insulin resistance, hyperinsulinemia and hypertension. 815 79

Plasma lipoprotein levels and carotid-femoral pulse wave velocity, used as a marker of aortic rigidity, were evaluated in 53 young subjects with borderline hypertension by comparison with normotensive controls of the same age and body surface area. Subjects with body weight excess, exaggerated alcohol intake, and/or tobacco consumption were excluded from the study. Borderline hypertensive patients were characterized by significantly higher values of pulse wave velocity and plasma levels of glucose, total cholesterol, high density lipoprotein subfraction HDL3, apolipoprotein B, and lipoprotein (a). There were no group/sex interactions. A significant dyslipidemia was observed in 13 males of the 53 borderline hypertensive subjects. Only in this subgroup did subjects exhibit a strong positive relationship between pulse wave velocity and either plasma total cholesterol or apolipoprotein B. The correlation was observed even after adjustment for blood pressure. The study provides evidence that, in young males with borderline hypertension, some abnormalities of plasma lipoproteins requiring treatment may be present and are associated with an increased stiffness of the arterial wall.
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PMID:Abnormalities of lipid metabolism and arterial rigidity in young subjects with borderline hypertension. 817 14

The objective of this study was to identify abnormalities in lipid and carbohydrate metabolism in women taking thiazide diuretics and determine whether these abnormalities are mitigated by concurrent postmenopausal estrogen replacement therapy. The study design was cross-sectional; its setting was Rancho Bernardo, an upper middle-class community in southern California. The subjects included 1047 white nondiabetic postmenopausal women, aged 50-89 yr, categorized by the use of thiazide diuretic, estrogen replacement therapy, both, or neither. Medical history including behavior, verified medication use, height, weight, fasting chemistry and lipid panels, and a standardized oral glucose tolerance test with fasting and 2-h plasma glucose and serum insulin levels were determined. Compared with nonusers, women taking thiazides had significantly lower high density lipoprotein cholesterol levels and significantly higher fasting triglyceride, glucose, and insulin levels. Concomitant use of thiazide and estrogen yielded lipid profiles and fasting glucose and insulin levels similar to those of subjects receiving estrogen alone, i.e. elevated high density lipoproteins, decreased low density lipoproteins, and lower levels of fasting glucose and insulin compared with those in nonusers. However, thiazide-associated postchallenge glucose and insulin elevations were not modified by estrogen. These patterns were not explained by differences in age, body mass index, exercise, smoking, alcohol use, type or dose of thiazide diuretic, type of estrogen replacement, or serum potassium levels. We conclude that postmenopausal estrogen use masks thiazide-associated dyslipidemia and fasting elevations in glucose and insulin levels, but does not improve thiazide-associated postchallenge glucose intolerance and hyperinsulinemia. Modification of most of the untoward metabolic effects of thiazides in women taking postmenopausal estrogen could provide a new incentive for the use of this traditional antihypertensive in elderly women.
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PMID:Thiazide-associated metabolic abnormalities and estrogen replacement therapy: an epidemiological analysis of postmenopausal women in Rancho Bernardo, California. 817 60

Hyperinsulinemia, insulin resistance, or both have been described in patients with essential hypertension. Previous work from our laboratory has shown that in hypertensive patients with microalbuminuria, dyslipidemia and abnormal patterns in the diurnal variations of blood pressure are frequently associated. Whether hyperinsulinemia and microalbuminuria are directly related has not been determined. To test this possibility, we measured the plasma insulin response to an oral glucose load in 25 patients with or without microalbuminuria and 20 normotensive control subjects. Serum lipid profile and 24-hour ambulatory blood pressure were obtained. In the hypertensive patients as a group, the plasma insulin response to glucose (evaluated as the insulin area under the curve) was significantly enhanced compared with a group of 20 normotensive healthy control subjects (46,311 +/- 3745 and 27,557 +/- 2563 pmol/L x 2 hours, P < .01). When the hypertensive patients were subdivided according to their albumin excretion rate, the microalbuminuric patients had significantly higher plasma glucose (969 +/- 45.2 versus 762 +/- 28.7 mmol/L x 2 hours, P < .01) and insulin (59,172 +/- 5964 versus 37,737 +/- 3422 pmol/L x 2 hours, P < .01) area under the curve values. In addition, a significant direct correlation was found to exist between insulin area under the curve and the urinary albumin excretion rate (r = .63, P < .001). Serum levels of lipoprotein(a) were significantly greater (P < .01) in patients with than in those without microalbuminuria and in control subjects. Furthermore, daytime diastolic blood pressure and nighttime systolic and diastolic blood pressure values were greater in patients with than in those without microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated serum insulin levels in patients with essential hypertension and microalbuminuria. 820 63

The effects of long-term monotherapy with felodipine, a calcium antagonist, on blood pressure, glucose tolerance, and serum lipid profiles were prospectively investigated in 51 hypertensive patients: 13 with normal glucose tolerance and 38 with glucose intolerance. The levels of plasma glucose, serum lipids, and glycosylated hemoglobin A1c were determined before and during long-term (7.5 +/- 0.5 months; range, 6 to 9 months) therapy with felodipine. A 75-g oral glucose tolerance test was performed before and during long-term felodipine therapy. Significant decreases in both systolic and diastolic blood pressures in both patient groups were maintained during the therapy. Neither fasting nor post-glucose load venous plasma glucose levels were altered in either group of patients, and no patients with normal glucose tolerance developed diabetes mellitus during the study. Serum lipid levels did not change significantly in either group of patients except for significant decreases in high-density lipoprotein cholesterol and apolipoprotein A-I in the group with normal glucose tolerance tests, but those changes remained within the normal range. Furthermore, neither serum lipid nor apolipoprotein levels were altered, even in patients with hypercholesterolemia (total cholesterol levels, > 5.69 mmol/L = 220 mg/dL). These results suggest that long-term therapy with felodipine may not alter glucose and lipid metabolism in hypertensive patients, and felodipine appears to be useful as an antihypertensive agent for hypertensive patients with either dyslipidemia or impaired glucose metabolism.
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PMID:Felodipine therapy may not alter glucose and lipid metabolism in hypertensives. Felodipine Multicenter Prospective Study Group in Japan. 828 62

Peripheral insulin resistance with normal glucose homeostasis and compensatory hyperinsulinemia is a common feature of a series of conditions. It is usually present in obesity and initiates the events leading to non insulin dependent diabetes. It is also pathogenetically related to hypertension, dyslipidemias and clinical atherosclerosis, diseases that are frequently associated between them. Although its etiology remains partially unknown, strong evidences suggest that it is due to a post receptor defect, involving the intracellular signals that drive carbohydrate metabolism. This explains the preservation of other insulin actions and the effect of hyperinsulinemia on hypertension, dyslipidemia and atherogenesis. In obesity, the increased lipid oxidation and serum free fatty acid levels, inhibit enzymes and cofactors involved in carbohydrate metabolism. This leads to a reduction in glucose disposal and increases hepatic glucose output, outlining a post receptor defect leading to insulin resistance.
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PMID:[Insulin resistance]. 830 18

Hypertension and diabetes appear to increase coronary heart disease risk in part by causing an abnormality in lipid metabolism. Most affected are patients with familial dyslipidemic hypertension (FDH) and noninsulin-dependent diabetes mellitus (NIDDM). The lipid disorders most often encountered in these patients are increased levels of triglycerides, very low-density lipoprotein (VLDL) cholesterol, and small, dense low-density lipoprotein (LDL) cholesterol, and low levels of high-density lipoprotein (HDL) cholesterol. These abnormalities appear to result from increased hepatic secretion of VLDL particles due to increased concentrations of free fatty acids and glucose, reduced VLDL clearance due to reduced activity of lipoprotein lipase, and reduced LDL clearance due to glycosylation of ligand proteins. Treatment of the dyslipidemia associated with FDH should follow the guidelines from the National Cholesterol Education Program. Treatment in men and women with NIDDM should be considered when LDL cholesterol levels are 130 mg/dl or above, triglyceride levels are 200 mg/dl or above, or non-HDL cholesterol levels are 160 mg/dl or greater. Aggressive lifestyle changes should be initiated first, including weight loss in obese patients, control of glucose levels in those with NIDDM, avoidance of antihypertensive drugs that may worsen lipid levels in patients with FDH, and eating a diet restricting saturated fat and cholesterol. Addition of lipid-altering drugs should be considered if such changes do not achieve effective lipid control. The agent should be tailored to the patient's lipid profile, in general by using bile acid resins, niacin, or reductase inhibitors to lower LDL cholesterol and gemfibrozil or niacin to lower triglycerides. Niacin should be avoided in patients with NIDDM.
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PMID:Understanding and treating dyslipidemia associated with noninsulin-dependent diabetes mellitus and hypertension. 836 60

Already in 1988 Raeven mentioned a syndrome of resistance to insulin (X-syndrome). Before and after that description, several studies featured the central role of tissue resistance to the effects of endogenous insulin during development of diverse biological disturbances: adipositas, intolerance to glucose (or diabetes mellitus), arterial hypertension, dyslipidemia, atherosclerosis. The author summarizes the available literature on this 'new' syndrome that has hitherto not yet been accepted by all scientists. However, although data so far do not always coincide, many recent results give evidence for the importance of the role of a fateful span: resistance to insulin (probably of genetic origin) and secondary hyperinsulinemia. Their role in the genesis of the above-mentioned clinical disturbances is described, as measures for 'physiological' therapy are stressed: strict diet and regular physical exercises. If these simple measures fail, special drugs may be effective.
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PMID:[Syndrome "X"]. 837 81


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