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Query: UMLS:C0020473 (hyperlipidemia)
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Abdominal obesity is closely associated with risk factors for cardiocerebrovascular disease and NIDDM and the precipitation of these diseases. Together, they seem to constitute a metabolic syndrome where hyperinsulinaemia, insulin resistance, hyperlipidaemia, hypertension, visceral fat accumulation, cardiocerebrovascular disease and NIDDM are the individual constituents. The background to this syndrome might be a primary aberration expressing itself as an increased sensitivity of the hypothalamo-adrenal axis, and subsequent inhibition of sex steroid hormone secretions. This in turn will probably be followed by metabolic derangements, primarily peripheral insulin resistance, as well as by visceral fat accumulation by mechanisms which are partially visualized by recent work in the field. Visceral fat accumulation may then amplify the metabolic aberrations via hepatic effects of excessive concentrations of portal FFA, producing hyperproteinaemia, hyperglycaemia, hyperinsulinaemia and, perhaps, hypertension. The background to the central endocrine aberration remains more speculative, but factors leading to increased cortisol production, including specific stress reactions, tobacco smoking and alcohol may turn out to be important. The tentative conclusion provides a hypothesis for further work, and has recently obtained considerable support from further observations in humans in other than the endocrine and metabolic areas, as well as from studies in experimental animal models, where such factors can be studied under fully controlled conditions, which is not possible in humans for ethical reasons.
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PMID:Regional fat distribution--implications for type II diabetes. 133 83

Hypertension has previously been suggested to be a part of a metabolic syndrome also involving hyperlipidemia, hyperinsulinemia, and decreased insulin sensitivity. In the present study, 10 untreated hypertensive subjects were challenged with a high-salt diet (20 g NaCl) for 1 week after 7 days on a low-salt diet (less than 3 g). The difference in mean blood pressure (MBP) at the end of the high-salt diet v the low-salt diet was denoted salt sensitivity. We related the salt sensitivity to indices of glucose and lipid metabolism and studied the effect of salt deprivation on these metabolic variables. Salt sensitivity was found to be significantly correlated to HDL cholesterol (r = 0.79, P less than .007), insulin sensitivity (M value at the euglycemic clamp, r = 0.68, P less than .003), and fasting serum insulin (r = 0.69, P less than .04). Salt deprivation induced an increase in fasting insulin (P less than .03), but did not significantly affect any other indices of glucose and lipid metabolism. In conclusion, our study shows that hyperinsulinemia, decreased sensitivity to insulin, and low levels of HDL cholesterol were most commonly seen in hypertensive subjects with a low sodium sensitivity. A putative mechanism might be an increased activity in pressor systems also affecting glucose and lipid metabolism.
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PMID:Metabolic cardiovascular risk factors and sodium sensitivity in hypertensive subjects. 138 59

Data from a health screening survey with over 18,000 adult participants were used to determine the relations between serum calcium concentration and the cardiovascular risk factors hypertension, hyperglycaemia, and hyperlipidaemia. Blood pressure and serum glucose and cholesterol concentrations were all positively related to each other independent of age, sex, kidney function, and obesity. Similar relations between the risk factors were found in subjects with hypertension or hyperglycaemia independent of the degree of overweight. These results suggested that there might be a metabolic syndrome of cardiovascular risk factors. Serum calcium concentration was positively related to systolic and diastolic blood pressures and serum glucose and cholesterol concentrations. Thus a common feature in the syndrome is an increased serum calcium concentration. The relations between serum calcium concentrations and the cardiovascular risk factors were not limited to the upper parts of the distribution, being seen over a wide range. Changes in calcium metabolism seem to be related to a metabolic syndrome of hypertension, impaired glucose tolerance, and hyperlipidaemia.
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PMID:Relation of serum calcium concentration to metabolic risk factors for cardiovascular disease. 314 67

A large segment of the population gradually develops insulin resistance, and the related metabolic syndrome is one of the most frequent causes of atherosclerosis. Searching for a practical indicator of insulin resistance, we studied the correlations between fasting serum insulin level, the general manifestations of insulin resistance syndrome, and various aspects of coronary artery disease in 797 men and 322 women. After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). We also noted a higher prevalence of hypertension, diabetes mellitus, and type IV hyperlipidemia. Significantly more women in the fourth than in the first quartile had angiographically documented significant stenosis of the coronary arteries (p = 0.0016, odds ratio 2.9, 95% confidence interval 1.5 to 5.6) and previous myocardial infarction (p = 0.0297, odds ratio 2.1, 95% confidence interval 1.1 to 4.1). Men in both the first and the fourth quartile had a more disturbed lipid profile and a higher prevalence of significant stenoses of coronary arteries and/or previous myocardial infarction than women; there was a tendency toward a lower prevalence of alcohol consumption (p = 0.0503), a higher prevalence of gout (p = 0.0634), and previous myocardial infarction (p = 0.0791) in men in the fourth than in the first quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

Epidemiological studies have revealed that elevated fibrinogen concentrations are associated with an increased risk of myocardial infarction, stroke, intermittent claudication, and cardiovascular mortality. The manner in which fibrinogen operates in atherogenesis has not yet been elucidated, but genetic control of fibrinogen levels is partially responsible. Fibrinogen frequently acts in concert with hyperlipidemia, diabetes, hypertension, physical inactivity, and age, variables that are influenced by insulin action. Because the offspring of hypertensive men tend to be hyperinsulinemic and insulin resistant from a young age, we hypothesized that their increased fibrinogen levels might reflect decreased insulin action and thus play a role in the metabolic syndrome. We chose 48 adult offspring (mean age, 38.4 years) of 30 fathers who had been treated for hypertension, and the former were matched by age, body mass index, sex, and smoking habits with 37 control subjects. Elevations in fibrinogen concentration (3.63 +/- 0.93 versus 2.87 +/- 0.54 g/L, P < .001) paralleled increases in blood glucose and insulin levels, estimates of insulin resistance, and blood pressure. In the offspring, in contrast to the control group, correlations between fibrinogen and metabolic-syndrome variables (ie, insulin, glucose, and waist and hip circumferences) were found. In stepwise multiple regression analyses, age and smoking habits were entered as variables in both study groups, but postload insulin and high-density lipoprotein cholesterol were entered as variables in the offspring group only. We propose that familial predisposition influences the relationship between insulin concentration and fibrinogen, an effect that may contribute to the clinical importance of the metabolic syndrome.
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PMID:Increased fibrinogen levels in the offspring of hypertensive men. Relation with hyperinsulinemia and the metabolic syndrome. 748 47

The metabolic syndrome is characterized by cluster-like occurrence of various risk-factors for vascular disease: overweight, hypertension, hyperlipidemia, hyperproteinuria. In the pathogenesis of this syndrome the peripheral resistance to insulin leading to hyperinsulinemia plays most likely a central role, as the development of individual components of the metabolic syndrome may causally be explained in this way. Various possible explanations exist for the development of insulin resistance: on the receptor level, as a result of changes in the capillary bed or in muscle fiber composition, or resulting from disturbed circulation of muscles. Clinical symptoms of hyperinsulinemia are hypertension, lipodystrophy, and type II diabetes. Patients with metabolic syndrome represent a group at high risk for arteriosclerotic vascular disease. Therapy aims primarily at reduction of hyperinsulinemia as the underlying factor. In particular non-medical intervention plays an important role (reduction of body weight, exercise). In drug therapy of hypertension only such antihypertensives which remain neutral to metabolism should be applied, i.e., ACE-inhibitors which even improve the metabolic condition.
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PMID:[ACE inhibitor in metabolic syndrome]. 785 77

Major cardiovascular risk factors, such as hypertension, hyperlipidemia, and diabetes, often cluster in the same individuals. It has been claimed that obesity, hyperinsulinemia, insulin resistance, and a deranged intracellular handling of ions have pathogenetic importance in the development of this metabolic syndrome. However, a decrease in peripheral blood flow is another factor found in all the different facets of this syndrome. An increased peripheral resistance and a rarefaction of skeletal vessels are often seen in hypertensive subjects. Also, the insulin resistance so commonly seen in hypertension may be a consequence of a decreased blood flow because insulin resistance is associated with a decreased capillarization in skeletal muscle. Furthermore, the activity of skeletal muscle lipoprotein lipase, the key enzyme involved in the removal of triglycerides from the circulation, is known to be related to skeletal muscle vascularization. Because enhanced sympathetic activity has been associated with vascular hypertrophy and rarefaction of vascularization, overactivity in this part of the autonomic nervous system may lead to structural changes that will decrease the blood flow in peripheral tissues and thereby induce the metabolic syndrome of cardiovascular risk factors, particularly in individuals who, for genetic reasons, have decreased capillarization at the onset.
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PMID:Decreased peripheral blood flow in the pathogenesis of the metabolic syndrome comprising hypertension, hyperlipidemia, and hyperinsulinemia. 848 Jun 20

Obesity is a multifactorial heterogenous condition. The location of excess fat on the body determines the risk of morbidity and mortality for significant disease. Visceral, or intraabdominal, fat is the fat depot most highly associated with illness and death from cardiocerebrovascular disease and diabetes. Visceral fat is also associated with a quartet of metabolic disturbances. Referred to as the metabolic syndrome, these abnormalities include hypertension, hyperlipidemia, hyperinsulinemia, and insulin resistance. The metabolic syndrome is also present in Cushing's syndrome, which is characterized by primary hypercortisolism as well as profound visceral adiposity and obesity. The interrelationship between hyperactivation or hypersensitivity of the stress axis and disease can be elucidated by an understanding of the effect of excess glucocorticoids upon energy storage and metabolism. The complex interactions of the stress axis upon the growth and reproductive axes, as well as upon the adipose tissue, suggest that chronic stress, whether psychological and/or physical, exerts an intense effect upon body composition, which, in turn, significantly affects the longevity and survival of the organism.
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PMID:Hypercortisolism and obesity. 859 40

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

Marked changes in the plasma concentration of several non-glucose monosaccharides have been detected among patients++ with end-stage renal disease. To find changes specific to renal disease and not caused by a failing urinary excretion, we studied the plasma monosaccharide concentration in patients with early-stage glomerulonephritis whose renal function was normal or only mildly compromised. Plasma mannose, fructose and 1,5-anhydroglucitol (1,5-AG) concentrations were measured using gas chromatography/mass spectrometry and isotope-labelled sugar standard additions. The daily urinary protein excretion was positively correlated with the plasma cholesterol (r = 0.785), mannose (r = 0.550), triglyceride (r = 0.531 ) and fructose (r = 0.401) concentrations, while the correlation with 1,5-AG (r = -0.581) was inverse. The correlations were statistically significant. As previous studies have revealed a close positive correlation between the plasma mannose and glucose concentrations, we calculated the mannose/glucose concentration ratio to find out whether the increase in mannose concentration was or was not explained by ambient glucose. There was a strong correlation between the ratio and the urinary protein excretion (r = 0.704). It is inferred that the metabolic syndrome associated with glomerulonephritis and characterised by hyperlipidemia also involves a derangement in mannose and 1,5-AG metabolism.
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PMID:Proteinuria and plasma hexosugars in early-stage glomerulonephritis. 886 96


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