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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Essential hypertension in patients with the metabolic syndrome is regularly associated with other metabolic disorders. Thus, most hypertensives are overweight and have a glucose intolerance, while many have concomitant hyperproteinemia and dyslipoproteinemia. Up until fairly recently, it was not known that so-called insulin resistance is a common denominator both of metabolic risk factors and hypertension. In recent years, our knowledge about insulin resistance has spawned an equally convincing and fascinating multidimensional concept which reveals and plausibly explains complex relationships between metabolism, hypertension and the coronary risk.
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PMID:[Hypertension in metabolic syndrome. Etiology and consequences]. 148 16

Insulin resistance and consecutive hyperinsulinemia in individuals with the metabolic syndrome are associated with dyslipidemia. This latter is characterised by hypertriglyceridemia and a diminishment of high-density lipoprotein (HDL) cholesterol in the plasma. In severe forms of insulin resistance, low density lipoprotein (LDL) cholesterol may also be elevated. Hypertriglyceridemia is due to an increase in the rate of synthesis of very low density lipoproteins (VLDL) in the liver, and a reduction in their breakdown by the lipoprotein lipase in non-hepatic tissue. Changes in VLDL metabolism are associated with a reduction in HDL concentrations. In addition, direct effects of insulin on the lipid metabolism have been described. Changes in lipid metabolism due to insulin resistance and hyperinsulinemia may be of significance for the atherosclerosis risk in patients with the metabolic syndrome.
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PMID:[Dyslipoproteinemia and metabolic syndrome. Effects of insulin resistance and hyperinsulinemia on lipid metabolism]. 148 17

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

Type 2 diabetes mellitus is characterized by impaired insulin release and sensitivity, elevated blood sugar and unfavourable changes in blood lipids. Insulin resistance and adverse blood lipids are also seen in the state of essential hypertension (the metabolic syndrome). Patients should learn to measure their own blood sugar. Treatment usually begins with regulation of the diet for 3-6 months. If this treatment fails, the next step is to give oral antidiabetic agents. Insulin treatment is required 1) when blood sugar is excessively high; 2) when oral agents fail; and 3) in case of increased need of insulin due to intercurrent disease. Antihypertensive treatment should not have adverse metabolic effects in patients with type 2 diabetes.
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PMID:[Treatment of non-insulin dependent diabetes (type 2 diabetes mellitus)]. 155 62

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

Insulin resistance associated with hyperinsulinemia (metabolic syndrome) emerged in recent years as an important health risk which is present in approximately 25% of the normal population in western industrialized societies. Insulin resistance as assessed for the whole body arises from a reduced glucose utilization of skeletal muscle. If the metabolic syndrome persists over a prolonged period of time, detrimental influences on the cardiovascular system become apparent involving diabetes mellitus, hypertension, and arteriosclerosis. Of particular pathogenic relevance is an unbalanced influence of insulin arising either from a diminished or enhanced insulin action depending on whether the various tissues of the body exhibit a reduced or unchanged insulin sensitivity. Since insulin resistance and hyperinsulinemia appear to be affected by various lifestyle factors, the unique opportunity exists of reducing cardiovascular mortality by correcting this syndrome at a time when degenerative changes have not occurred in the cardiovascular system. Of great importance is the finding that dietary factors can have a modulatory action on insulin sensitivity. In animal experiments, an increased intake of (saturated) fat and refined carbohydrates increased insulin resistance. Since psychosocial distress is expected to be associated with a sustained activation of the sympathoadrenal axis, it is likely also to aggravate the metabolic syndrome. A factor with a beneficial action appears to be physical exercise. In view of the high incidence of cardiovascular diseases, further research on lifestyle factors with an insulin-sensitizing or insulin-desensitizing action is required. Of prime importance is the reevaluation of established dietary recommendations and diets should be designed which take into account the individual cardiovascular risk factor profile.
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PMID:Insulin resistance, hyperinsulinemia, and cardiovascular disease. The need for novel dietary prevention strategies. 159 Jul 42

Dependent on the dosages used, digestion and absorption inhibitors or disaccharidase inhibitors, such as Acarbose, might cause malabsorption of nutrients, and hence, among other effects, affect caloric balances. This negative effect on caloric balance has actually been well documented in animal experimentation. However, in nondiabetic subjects with excessive degrees of obesity, no consistent weight reduction could be induced by disaccharidase inhibitors. Subsequently, Acarbose has been advocated for type 2 diabetic patients in dosages that might reduce postprandial hyperglycemia and insulinemia, whereas significant degrees of malabsorption should be excluded. At these dosages of the drug, there is no clinical perspective with regard to weight-reducing (side) effects of disaccharidase inhibitors. Whether a hypothetical diminution of serum insulin daily profiles during Acarbose treatment in obese type 2 diabetic patients might contribute to a normalization of the metabolic syndrome and to a facilitation of weight-reducing efforts remains speculative. At present, there does not seem to be much rationale in trying to exploit digestion and/or absorption inhibitors for weight-reduction therapies in obesity, unless they are used to enforce a negative caloric balance by malabsorption of nutrients.
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PMID:Pharmacological treatment of obesity: digestion and absorption inhibitors-clinical perspective. 172 47

Insulin resistance appears as the pathophysiological basis of metabolic syndrome and NIDDM. In type 2 diabetics additionally we observe a delayed and prolonged postprandial insulin response. These both processes represent a pathophysiological and pathogenetic unity of disturbances. The prevention and therapy of insulin resistance, metabolic syndrome and type 2-diabetes with diet involves 3 main issues: reduction of energy uptake and of body weight in obese; Composition of meals concerning the principles of fat reduced lactovegetabile nutrition; guaranteeing of longer postabsorptive phases (between meals), to avoid a permanent postprandial hyperinsulinemia and development of insulin resistance. Anti-insulin resistance diet is therefore a carbohydrate enriched, fat-reduced (lactovegetabile) nutrition with not too frequent meals (longer meal-free phases) and mainly reduced energy intake in overweight.
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PMID:[Treatment of type 2 (non-insulin dependent) diabetes and the metabolic syndrome with diet]. 177 27

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

While the incidence of essential hypertension is not increased in type 1 diabetics, it is about three times as high in type 2 diabetics. Since in 50% of the cases, hypertension is present before the metabolic disorder becomes manifest, an association between the etiologies of the two disturbances was suspected as long as 65 years ago. A new understanding of the significance of insulin resistance and hyperinsulinemia suggests that the two conditions are part of a single metabolic disorder. This is supported by the fact that normal-weight hypertensives can also manifest insulin resistance, and they more often develop a type 2 diabetes mellitus. These facts urge us to re-think our therapeutic approach to hypertension, and to employ, as far as possible, only those substances that have no negative influence on the incidence of the metabolic disorder. With the introduction of ACE-inhibitors capable of improving insulin sensitivity, we now have, for the first time, the possibility of improving the prognosis of the metabolic syndrome. Moreover, their molecular mechanism of action provides initial clues as to the possible etiology of the syndrome.
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PMID:[Essential hypertension and diabetes mellitus]. 218 85


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