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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several lines of evidence suggest that a subset of women may be at increased risk of cardiovascular disease because of unfavorable alterations in insulin action and/or production, accompanying altered apolipoprotein metabolism and altered androgenicity and/or estrogenicity. A number of cardiovascular disease risk factors, including central obesity, insulin resistance (with associated hyperinsulinemia), dyslipidemia, and/or diabetes mellitus, tend to cluster in these women. Another common ovarian morphology in women with hyperandrogenism is polycystic ovaries, which cluster with hirsutism, anovulation, infertility, gonadotropin secretion abnormalities, android fat distribution, and many important cardiovascular disease risk factors. Studies indicate that androgen excess may be a signal of increased risk for coronary artery disease, even in younger women. If androgenicity and insulin resistance are early warning signs of increasing risk of morbidity and mortality, these patients are prime candidates for preventive medicine. It is important that primary care providers begin to recognize these androgen disorders as a clue to the existence of a complex, lifelong pattern potentially placing women at risk for premature morbidity and mortality and initiate preventive treatment before irreversible thresholds are crossed.
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PMID:Obesity, lipids, cardiovascular risk, and androgen excess. 782 38

Despite recent progress in therapy and management of diabetes mellitus, diabetes remains a serious disease with life-threatening complications. It is by far the most common metabolic disease and affects 5% of the population in industrialized countries. Noninsulin-dependent diabetes mellitus (NIDDM) is a complex disorder characterized by insulin resistance and impaired insulin secretion and is associated with an increased risk of coronary heart disease, peripheral vascular disease, arterial hypertension and dyslipidemia. Predisposing factors for NIDDM are obesity and a family history of diabetes. Greater physical activity has been associated inversely with the prevalence of NIDDM in several cross-sectional studies. Physical activity increases the sensitivity to insulin, and regular endurance exercise can induce and maintain weight loss, improve glucose tolerance and ameliorate most of the abnormalities in the metabolic syndrome. Type I diabetes mellitus arises as a consequence of immunologically mediated pancreatic islet beta-cell destruction in genetically susceptible individuals. It is an insidious process that may occur over years. During the stage of disease evolution (prediabetes), individuals may be identified by the presence of immunological markers and a decline of beta-cell function. The autoimmune nature of the disease process has led to attempts to stop this process by immune intervention strategies. A variety of immune interventions has been used, some immunosuppressive and some immunomodulatory. Several screening programs are used in order to identify high-risk subjects (i.e. first-degree relatives of individuals with type I diabetes) who may benefit from an early intervention. The ultimate goal of all these efforts is to prevent the development of overt type I diabetes mellitus in those at risk for the disease, using strategies that are both safe and specific. This review summarizes the results of the various studies conducted to date and outlines the approaches currently being tested.
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PMID:[Is prevention of diabetes mellitus possible?]. 783 27

To investigate the pathogenesis of hypertension in patients with obesity and insulin resistance and to explore the role of plasma lipids, we studied 30 subjects at the end of 7 days of low (20 mEq/d) then high (200 mEq/d) sodium diets. Glucose and insulin tolerance tests were performed at the end of each week and blood and urine collected for measurements of plasma aldosterone, renin activity, electrolytes, insulin, and lipoproteins. There was a strong negative correlation between plasma aldosterone and high-density lipoprotein cholesterol during both diets. There were weaker positive correlations between plasma aldosterone and insulin or triglycerides. When the aldosterone-renin ratio was the dependent variable and the correlation controlled for serum potassium, the inverse relationship with high-density lipoprotein cholesterol and the positive correlation with insulin remained, but only during the high salt diet. Subjects were divided into three groups based on high-density lipoprotein cholesterol. Subjects with the lowest high-density lipoprotein cholesterol levels showed the highest aldosterone, plasma triglycerides, body mass index, and waist-to-hip ratio. Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. There was a weak direct correlation between plasma aldosterone and systolic blood pressure during the high salt diet. These data suggest that high aldosterone levels may be a link between dyslipidemia, insulin resistance, and hypertension, a relationship made more evident by high salt intake.
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PMID:Relationships among plasma aldosterone, high-density lipoprotein cholesterol, and insulin in humans. 784 50

The individual components of the metabolic syndrome such as central obesity, dyslipidemia with increased triglycerides and decreased HDL-cholesterol, hyperuricemia, hypertension and progressive glucose intolerance are markers for an increased risk of atheroma and type 2 (non-insulin-dependent) diabetes. All components, with the exception of hyperuricemia, are associated with skeletal muscle insulin resistance, leading to compensatory chronic hyperinsulinemia. Insulin resistance/hyperinsulinemia, in turn, is associated with a series of hypertensiogenic and atherogenic side effects, aggravating the individual components of the metabolic syndrome. From a more pathophysiologically orientated point of view, early identification of individuals obviously at risk for atheroma and type 2 diabetes, as well as early intervention aimed at the improvement of reduced insulin action may play a central role in an integrated life-style approach of primary prevention of atherosclerosis and type 2 diabetes.
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PMID:[The metabolic syndrome. Pathophysiologic causes, diagnosis, therapy]. 784 93

Several epidemiologic and clinical studies over the past years have shown that insulin resistance and hyperinsulinemia are related to dyslipidemia, hypertension, android obesity and non-insulin-dependent diabetes mellitus (NIDDM). The insulin-resistance syndrome is thus closely associated with a cluster of potent cardiovascular risk factors, thereby explaining the 3-4 times higher incidence of cardiovascular disease in NIDDM. Recent observations point to the fact that insulin resistance is genetically determined and can be diagnosed a long time before the clinical manifestation of diabetes mellitus in the prediabetic stage (stage of hyperinsulinemia, hypertension and hyperlipidemia). Hence, it is not surprising that many NIDDM subjects suffer from cardiovascular complications already at the time diabetes is diagnosed. The pathogenetic mechanism of insulin resistance/hyperinsulinemia as cardiovascular risk factor is considered to be a direct atherogenic action of insulin on vessel wall cells and an indirect effect on upper body obesity, blood pressure, lipids and hemostasis.
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PMID:[Insulin resistance and cardiovascular complications]. 784 94

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

Coronary heart disease remains the most common cause of death among men and women in the United States. With an estimated cost of $56 billion annually for the treatment of heart disease, and an increasing prevalence due to aging of the population, both primary and secondary prevention of coronary heart disease take on major public health importance. New insights into the relationship between smoking, hypertension, physical activity, dyslipidemia, obesity, hyperinsulinemia and diabetes mellitus, clotting factors, and alcohol and the subsequent development of coronary heart disease are reviewed and means of intervention are highlighted. The role of aspirin, beta-blockers, calcium-channel blockers, antiarrhythmics, and angiotensin-converting enzyme inhibitors in the secondary prevention of myocardial infarction are briefly reviewed and the potential role of hormone replacement therapy in women is discussed.
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PMID:Primary and secondary prevention of ischemic heart disease. 791 86

Lipoprotein lipase (LPL), a 55 kDa secretory glycoprotein produced in numerous tissues, is a hydrolytic enzyme, rate-limiting for the removal of lipoprotein TG from the circulation. It is activated by apoprotein CII present on TG-rich lipoproteins. It is involved in lipid transfer between lipoproteins, and plays an important role in the formation of HDL. The fate of LPL-derived lypolysis products differs between tissues: for instance, in adipose tissue, LPL-mediated delivery of free fatty acids is rate-limiting for TG storage, whereas in muscle it provides an alternate source of lipid fuel. LPL is regulated by hormones like insulin and nutrients; its activity depends on the metabolic state of the tissue. It has distinct roles in many normal tissues, such as adipocytes or muscles, as well as an important role in atherogenic dyslipidemia and in metabolic diseases including obesity and hypertriglyceridemia.
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PMID:[Lipoprotein lipase: a key enzyme of lipid metabolism]. 793 19

The insulin resistance syndrome (IRS) is characterized by a constellation of interrelated coronary heart disease (CHD) risk factors, including dyslipidemia, obesity, central obesity, elevated systolic blood pressure, and hyperinsulinemia. Factor analysis was used to investigate the clustering of these risk factors in individuals by examining the correlational structure among these variables. Data from 281 genetically unrelated nondiabetic women who participated in exam 2 (1979 to 1980) of the Kaiser Permanente Women Twins Study were used. Factor analysis reduced 10 correlated risk factors to 3 uncorrelated factors, each reflecting a different aspect of the IRS: factor 1 (increased body weight, waist circumference, fasting insulin, and glucose), factor 2 (increased postload and fasting glucose and insulin and systolic blood pressure), and factor 3 (larger low-density lipoprotein particles, decreased plasma triglycerides, and increased high-density lipoprotein). Together, the factors explained nearly 66% of the total variance in the data. Thus, factor analysis defined three distinct aspects of the IRS in this sample of nondiabetic women. These factors may reflect separate underlying mechanisms of the syndrome, each of which may also be involved in CHD risk.
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PMID:Multivariate analysis of the insulin resistance syndrome in women. 798 Nov 83

Hypertension is often related to metabolic disorders, such as android obesity, glucose intolerance, dyslipidemia, and hyperinsulinism (X syndrome). Insulin resistance (IR), described as the common link among these disorders, could contribute to an increase in coronary risk. The euglycemic insulin clamp technique has been used to show that different classes of antihypertensive agents have different effects on IR. The purpose of this multicenter study was to compare the effects of captopril to those of nicardipine on insulin profile using the oral glucose tolerance test (OGTT), a routine-feasible test. After a 1-month single-blind placebo period, 154 patients with hypertension and android obesity were randomized to 3 months of double-blind therapy with either 50 mg captopril twice daily (n = 77) or 50 mg nicardipine twice daily n = 77). An OGTT with an assay of insulin was performed before and after active treatment. Lipid parameters, Factor VII (F VII), fibrinogen, plasminogen activator inhibitor 1 (PAI-1), and insulin-like growth factor I (IGF-I) were measured at the same time. After 3 months of treatment, the changes from baseline in mean +/- SD values for the insulin area under the curve (AUC) were -24.8 +/- 107.4 microIU x h/mL (-15.2%) for captopril v 6.1 +/- 98.6 microIU x h/mL (4.8%) for nicardipine (P = .072). Changes in peak insulin values were -18.3 +/- 86.2 microIU/mL (-14%) for captopril v 6.7 +/- 79.4 microIU/mL (6.6%) for nicardipine (P = .070).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the effects of captopril and nicardipine on insulin sensitivity and thrombotic profile in patients with hypertension and android obesity. CaptISM Study Group. Captopril Insulin Sensitivity Multicenter Study Group. 798 64


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