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 65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have indicated that the waist/hip circumference ratio (WHR), an index of abdominal fat distribution, is a risk factor for cardiovascular disease and diabetes, in parallel with other previously established risk factors. Obesity, without taking fat distribution into account, seems to be associated with WHR in its relationship to the metabolic risk factors for these diseases. The important component of the WHR is probably the mass of visceral fat. This cluster of phenomena constitute what has recently been called the metabolic syndrome or syndrome X. Visceral fat mass is probably increased by a multiple endocrine aberration, where steroid hormones are important. This seems to cause insulin resistance by direct effects on the periphery, which may be amplified by the metabolism of the enlarged visceral adipose tissues.
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PMID:Abdominal fat distribution and the metabolic syndrome. 128 66

Clinical and epidemiological findings over the last few years are increasingly pointing to a metabolic syndrome comprising major cardiovascular risk factors, which frequently characterizes type II diabetes and its preliminary stages. More recent studies have shown that insulin resistance is genetically determined and can be detected in a pre-diabetic stage long before diabetes mellitus becomes manifest. It is thus not surprising that a large percentage of patients with type II diabetes already have clear signs of arteriosclerosis at the time the diagnosis is made. The results of the Schwabing study II indicate a "point of no return" for the development of cardiovascular disease, which makes early and vigorous intervention involving all facets of the metabolic syndrome a matter of urgency.
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PMID:[Metabolic syndrome and type-II diabetes. Relations to macroangiopathy]. 148 15

Epidemiological studies have documented the association between cardiovascular disease and high blood pressure, dyslipidaemia, impaired glucose tolerance, non-insulin-dependent diabetes mellitus (NIDDM), and central obesity. In fact, several of these abnormalities, often all of them, can be identified in the very same individuals, constituting the entity of the multiple metabolic syndrome. Furthermore, many of these abnormalities seem to run in families. These findings raise important questions about the genetic epidemiology of the disease and about the molecular genetic background of the most likely common nominator of this syndrome, namely insulin resistance. Therapeutic actions must also be carefully considered to avoid the encouragement of some abnormalities while treating others.
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PMID:Multiple metabolic syndrome: aspects of genetic epidemiology and molecular genetics. 148 39

Recent prospective, epidemiological research has demonstrated the power of an increased waist/hip circumference ratio (WHR) to predict both cardiovascular disease (CVD) and non-insulin dependent diabetes mellitus (NIDDM) in men and women. Obesity, defined as an increased total body fat mass, seems to interact synergistically in the development of NIDDM, but not of CVD. Increased WHR with obesity (abdominal obesity) seems to be associated with a cluster of metabolic risk factors, as well as hypertension. This metabolic syndrome is closely linked to visceral fat mass. Increased WHR without obesity may instead be associated with lift style factors such as smoking, alcohol intake, physical inactivity, coagulation abnormalities, psychosocial, psychological and psychiatric factors. Direct observations show, and the risk factor associations further strengthen the assumption, that abdominal (visceral) obesity is more closely associated to NIDDM than CVD, while an increased WHR without obesity may be more closely linked to CVD than NIDDM. It remains to be established to what extent, if any, an increased WHR in lean men, and particularly in lean women, indicates fat distribution. Other components of the WHR measurement might be of more importance in this connection.
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PMID:Abdominal fat distribution and disease: an overview of epidemiological data. 157 56

Many studies have shown that hyperinsulinemia and/or insulin resistance are related to various metabolic and physiological disorders including hypertension, dyslipidemia, and non-insulin-dependent diabetes mellitus. This syndrome has been termed Syndrome X. An important limitation of previous studies has been that they all have been cross sectional, and thus the presence of insulin resistance could be a consequence of the underlying metabolic disorders rather than its cause. We examined the relationship of fasting insulin concentration (as an indicator of insulin resistance) to the incidence of multiple metabolic abnormalities in the 8-yr follow-up of the cohort enrolled in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease in Mexican Americans and non-Hispanic whites. In univariate analyses, fasting insulin was related to the incidence of the following conditions: hypertension, decreased high-density lipoprotein cholesterol concentration, increased triglyceride concentration, and non-insulin-dependent diabetes mellitus. Hyperinsulinemia was not related to increased low-density lipoprotein or total cholesterol concentration. In multivariate analyses, after adjustment for obesity and body fat distribution, fasting insulin continued to be significantly related to the incidence of decreased high-density lipoprotein cholesterol and increased triglyceride concentrations and to the incidence of non-insulin-dependent diabetes mellitus. Baseline insulin concentrations were higher in subjects who subsequently developed multiple metabolic disorders. These results were not attributable to differences in baseline obesity and were similar in Mexican Americans and non-Hispanic whites. These results support the existence of a metabolic syndrome and the relationship of that syndrome to multiple metabolic disorders by showing that elevations of insulin concentration precede the development of numerous metabolic disorders.
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PMID:Prospective analysis of the insulin-resistance syndrome (syndrome X). 158 98

Epidemiological studies have clearly shown that the so-called metabolic syndrome which is linked to insulin resistance and a reduced glucose utilization of muscle represents an important risk factor for cardiovascular disease. However, only little is known of the intracellular consequences of insulin resistance. An important feature of an altered substrate utilization is related to signal transduction of gene expression. For the example of myosin heavy chain expression, it is shown that metabolic signals exist which reflect the fuel flux and substrate utilization of the heart muscle cell. The signals were characterized in functional states of the heart associated with altered metabolic influences (fasting, diabetes, sucrose feeding, increased calorie intake, carnitine palmitoyltransferase inhibition). In the pressure-overloaded heart, metabolic interventions which are expected to increase glucose utilization (sucrose feeding, captopril treatment) have a pronounced effect. Although a link with gene expression remains to be established, it should be noted that the sarcoplasmic reticulum Ca(2+)-pump activity seems to be affected in a functionally comparable manner. It is concluded that metabolic signals alter the protein phenotype of heart muscle and it is expected that a deranged signal transduction affects, not only the heart, but also vascular muscle.
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PMID:The metabolic syndrome and signal transduction of gene expression. 183 54

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

Evaluation of metabolic disturbances has had an important role in the modification of oral contraceptive formulations toward estrogen-progestin combinations with reduced adverse metabolic impact. An increasing number of interrelationships between metabolic risk factors for cardiovascular disease are being recognized, and a metabolic syndrome of disturbances has been identified with insulin resistance as a potential underlying factor. The insulin resistance syndrome includes hyperinsulinemia and impaired glucose tolerance, hypertriglyceridemia, reduced high-density lipoprotein concentrations, and hypertension. Increased concentration of a small, dense, low-density lipoprotein subtype may also be important. Depending on steroid type and dose, combined oral contraceptives may induce all the features of the insulin resistance syndrome. Reduction in estrogen dose and modification of progestin content have resulted in formulations with no adverse effect on high-density lipoprotein and blood pressure, but insulin resistance and hypertriglyceridemia remain. These are caused primarily by the estrogen component. Therefore modification of the estrogen content of oral contraceptives might result in "metabolically transparent" formulations that could conceivably afford a degree of cardiovascular protection.
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PMID:Update on the metabolic effects of steroidal contraceptives and their relationship to cardiovascular disease risk. 817 2

We have investigated the prevalence of cardiovascular risk factors including insulin and lipoprotein(a) in 40-year old men from the island of Oland (n = 314, 84% of those invited) in order to assess to what extent insulin and lipoprotein(a)--two of the currently discussed risk factors--correlated with each other, as well as with some of the more established risk factors. An inverse correlation was found in bivariate analyses between lipoprotein(a) and some of the risk factors for cardiovascular disease included in the 'metabolic syndrome' (triglycerides; r = -0.15, BMI; r = -0.18, and insulin/glucose ratio; r = -0.18) (p < 0.001). In multivariate analysis only the inverse correlation with triglycerides remained. Since lipoprotein(a) has been shown to be an independent risk factor for myocardial infarction, there may exist two subgroups of cardiovascular risk patients: one more obese, hyperinsulinaemic and with several metabolic derangements; and another comprising non-obese subjects with higher lipoprotein(a) values.
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PMID:Non-obese men with high lipoprotein(a) values--a cardiovascular risk group different from those with the metabolic syndrome? 819 5


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