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

For better comprehension of the metabolic syndrome, it is necessary to differentiate the effect of insulin on glucose metabolism on the one hand, and on other metabolic activities on the other hand. Whereas glucose utilization is affected by insulin resistance, the effect of insulin on lipid metabolism, ion and aminoacid transport does not seem to be diminished. Lipid metabolism, however, seems to play a crucial role in the induction of the vicious cycle. Increased energy and fat ingestion may be due to an increased number of galanin secreting cells in the hypothalamus. The excessive fat intake results in an increased rate of release of insulin and increased influx of triglycerides into the blood. From these triglycerides an excess of free fatty acids is released by the action of lipoprotein lipase. The increased plasma free fatty acid level then results in insulin resistance affecting glucose metabolism. Also, these free fatty acids may impair the secretion of insulin. Induction of insulin resistance results in higher glucose levels, which may cause hyperinsulinemia. Hyperinsulinemia maintains the elevation of triglycerides. When diabetes becomes overt and elevated glucose levels prevail, the hyperinsulinism acts on the metabolic pathways which are still sensitive to insulin, namely lipid metabolism, aminoacid transport and ion transport.
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PMID:Hyperinsulinemia, hyperproinsulinemia and insulin resistance in the metabolic syndrome. 864 79

The association between type A behavior and a cluster of parameters of the metabolic syndrome was studied in 919 randomly selected healthy young adults. Type A behavior was measured using the Type A Behavior Questionnaire for the Finnish Multicenter Study and the Hunter Wolf A-B Rating Scale. The results showed that type A men scored higher on the "Metabolic Syndrome Precursors Factor," representing a metabolic entity, than did non-type A men. In addition, type A behavior had a moderating effect on the relationship between parameters of the metabolic syndrome, that is, interdependence of these somatic factors was stronger in type A men than in non-type A men. These findings were not true of women. It is discussed whether type A behavior might affect bodily functions through increased activity along the pituitary-adrenal system resulting in insulin resistance, compensatory hyperinsulinemia, and other characteristics of the metabolic syndrome.
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PMID:Type A behavior and metabolic syndrome precursors in young adults. 867 82

A total of 359 Wanigelas from Papua New Guinea and 1041 Nauruans had urinary albumin concentrations (UAC), serum insulin, and a number of cardiovascular disease (CVD) risk factors measured during population-based surveys of non-insulin-dependent diabetes mellitus. These data were used to explore the hypothesis that microalbuminuria is closely associated with insulin resistance and the metabolic syndrome. In both Nauruans and Wanigelas, worsening glucose tolerance was associated with increasing prevalence of micro- and macroalbuminuria. Within each category of glucose tolerance, microalbuminuria was associated with general worsening of cardiovascular risk factors including lipid concentrations, blood pressure and obesity, although few of the associations were statistically significant. Correlations between UAC and markers of insulin resistance (fasting insulin, fasting insulin/glucose ratio and HOMAS%, a computer-modelled estimate of insulin sensitivity) were weak and inconsistent irrespective of glucose tolerance status. Relationships between insulin sensitivity and urinary albumin in normoglycaemic Wanigelas and Nauruans, and in diabetic Nauruans, were no longer significant after adjusting for fasting glucose and body mass index. While microalbuminuria in Nauruans and Wanigelas was associated with cardiovascular risk factors irrespective of glucose tolerance, it seems unlikely on the basis of these results that the relationship is mediated through a common association with insulin resistance.
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PMID:Microalbuminuria, cardiovascular risk factors, and insulin resistance in two populations with a high risk of type 2 diabetes mellitus. 873 26

In this paper we presented characteristics of insulin resistance syndrome (IRS), also known as metabolic syndrome and syndrome X, with an emphasis on insulin resistance in hyperandrogenemic women. The aim features of IRS are obesity, hypertension, dyslipidemia-hypertriglyceridemia and decreased HDL cholesterol, impaired glucose tolerance with hyperinsulinemia and higher cardiovascular morbidity. It is considered typical that in hyperandrogenemia, especially in PCO syndrome, insulin resistance and hyperinsulinemia without other characteristics of IRS are expressed.
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PMID:[Androgen excess in women and the metabolic syndrome (syndrome X)]. 875 4

Survivors of childhood cancer have been reported to have a severalfold increased risk of death from cardiovascular disease. A cluster of metabolic abnormalities, including obesity, insulin resistance, hyperinsulinemia, glucose intolerance, hypertension, and dyslipidemia, have been designated as forming a metabolic syndrome that is associated with increased cardiovascular mortality. We studied 50 survivors (23 males) of childhood cancer, aged 10.5-31.2 yr, an average of 12.6 yr (range, 7.9-21.3 yr) after their diagnosis and compared them with 50 age- and sex-matched controls for signs of the metabolic syndrome by examining clinical and anthropometric measures, serum lipid profile, and fasting plasma insulin and glucose concentrations. Spontaneous nocturnal GH secretion was also evaluated in the cancer survivors. The patients had increased relative weight (P = 0.03) and body fat mass (P < 0.001), decreased serum high density lipoprotein (HDL) cholesterol (P < 0.001), and a reduced ratio of HDL to total cholesterol (P = 0.01). Fasting plasma glucose and insulin levels were higher (P < 0.001 and P = 0.003, respectively) in the cancer survivors than in the controls. The patients had an increased risk [odds ratio (OR), 4.5; 95% confidence interval (CI), 1.3-15.8; P = 0.01] of obesity (relative weight, > 120%), fasting hyperinsulinemia ( > 111 pmol/L; OR, 3.0; 95% CI, 1.0-8.6; P = 0.04), and reduced HDL cholesterol ( < 1.07 mmol/L; OR, 7.9; 95% CI, 2.2 to 29.6; P < 0.001). A combination of obesity, hyperinsulinemia, and low HDL cholesterol was seen in eight cancer survivors (16%), but in none of the controls (P = 0.01). This high risk group was characterized by reduced spontaneous GH secretion (P = 0.02). Long term survivors of childhood cancer appear to have an increased risk of manifestations of the metabolic syndrome. Decreased GH secretion may contribute to these metabolic abnormalities.
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PMID:Long-term survivors of childhood cancer have an increased risk of manifesting the metabolic syndrome. 876 73

The predictive associations of Type A factors with changes in some essential parameters of the cluster of disorders known as metabolic syndrome (Syndrome X) were studied during a 3-year follow-up period in 1,147 randomly selected healthy adolescents and young adults. Type A behavior was measured with the Hunter Wolf A-B Rating Scale. Physiological parameters studied were serum insulin, high-density and low-density lipoprotein cholesterol, triglycerides (TG), systolic and diastolic blood pressure, body-mass index (BMI), subscapular skinfold thickness (SSF), and centrality index. Among the Type A factors in boys and men, high baseline Aggression predicted an increase in the individual parameters of metabolic syndrome (i.e., insulin, TG, SSF, and BMI) as well as a global aggravation of the cluster of metabolic parameters. In girls and women, increases in Eagerness-Energy and Responsibility across the 3 years of follow-up predicted an increase in serum insulin and a decrease in SSF, respectively.
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PMID:Type A factors as predictors of changes in the metabolic syndrome precursors in adolescents and young adults--a 3-year follow-up study. 878 37

The relations between life changes, locus of control and changes in the parameters of the metabolic syndrome were examined. A three-year follow-up study of 671 randomly selected, healthy adolescents and young adults was used. Somatic parameters measured both at the baseline and the follow-up were serum insulin, serum HDL chol, serum triglyceride, SBP and BMI. Locus of control was measured with the Nowicki-Strickland locus of control scale and subjects were asked about life changes that they had faced during the follow-up period. Results showed that, in women, there were significant main effects for life changes in predicting (high) somatic risk level, whereas, in men, an opposite association was found. In addition, locus of control had a moderating effect on the life change-metabolic parameters relation, i.e. most of the life changes predicted a lower level of somatic risk in subjects with an external rather than internal locus of control. Results question the universal applicability of beneficial health effects of internal locus of control. It was suggested that accumulation of life changes might contribute, in interaction with locus of control, to the early development of the metabolic syndrome.
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PMID:Life changes, locus of control and metabolic syndrome precursors in adolescents and young adults: a three-year follow-up. 881 10

The metabolic syndrome is a well-known risk for the development of cardiovascular disease. In the present study the possible importance of an altered visceral adipocyte beta-adrenoceptor function in this syndrome was investigated. In 65 subjects of both sexes undergoing elective surgery for non-malignant disorders, the metabolic syndrome phenotype and the lipolytic sensitivity for various beta-adrenoceptor subtype agonists in omental adipocytes were determined. The study group represented a wide range of abdominal adipose tissue distribution (waist-to-hip ratios 0.76-1.13), but was otherwise apparently healthy. The subjects were divided into three subgroups according to their waist-to-hip (WHR) ratios: 1) WHR < 0.92; 2) WHR 0.92-1.04; 3) WHR > 1.04. The subgroups demonstrated significant differences regarding body mass index, sagittal diameter, systolic and diastolic blood pressures, plasma concentrations of glucose, insulin, triglycerides and HDL-cholesterol (p = 0.005-0.0001). Furthermore, in omental adipocytes beta 3-adrenoceptor sensitivity, but not beta 1-and beta 2-adrenoceptor sensitivities, differed significantly between the WHR subgroups (p = 0.0001). beta 3-adrenoceptor sensitivity was also related to the other components of the metabolic syndrome, although a strong covariation between WHR and beta 3-adrenoceptor sensitivity vs blood pressure and the metabolic parameters was found. The present data provide evidence of a relationship between upperbody obesity and its associated metabolic complications and also, an increased visceral fat beta 3-adrenoceptor sensitivity. We suggest that the latter finding results in an augmented release of non-esterified fatty acids from the visceral fat depot to the portal venous system. This may in turn contribute to the development of the metabolic syndrome.
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PMID:The metabolic syndrome is related to beta 3-adrenoceptor sensitivity in visceral adipose tissue. 881 9

Aging is associated with an increased incidence of hypertension, noninsulin-dependent diabetes mellitus, and coronary heart disease. Because these conditions often cluster in the same individuals, there has been speculation that a common mechanism is responsible for all of these pathological states. Both epidemiological and clinical research has shown that insulin resistance and/or hyperinsulinemia are associated with glucose intolerance, dyslipidemia (high plasma triglyceride and low high-density lipoprotein-cholesterol levels), and higher systolic and diastolic blood pressures. Therefore, insulin resistance and hyperinsulinemia have been proposed as the causal link among the elements of the cluster mentioned above, now most commonly referred to as the insulin resistance syndrome, syndrome X, or the metabolic syndrome. The elderly are more glucose intolerant and insulin-resistant, but it remains controversial whether this decrease in function is an inevitable consequence of "biological aging" or the result of what might be referred to as environmental or lifestyle variables: increased obesity, a detrimental pattern of fat distribution, or physical inactivity that usually accompany age. All of these modifiable environmental factors have also been shown to result in increases in insulin resistance and hyperinsulinemia and are risk factors for the development of the diseases of the metabolic syndrome. Recent interventional studies that have attempted to reverse these conditions in the elderly have shown improved insulin sensitivity, and glucose tolerance. Insulin secretion, on the other hand, seems to decrease with age even after adjustments for differences in adiposity, fat distribution, and physical activity. This may be responsible for the glucose intolerance in the very old even after improvements have been made in their lifestyle variables.
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PMID:The effect of age on insulin resistance and secretion: a review. 882 67

The effects of antihypertensive drugs on cardiovascular metabolic risk factors were monitored in 42 patients with essential hypertension (diastolic blood pressure [DBP] >95 mm Hg). In a double-blind randomized parallel-group study, they were treated with atenolol 50 mg once per day (n = 25) or urapidil 60 mg twice per day (n = 17), a peripheral alpha1-receptor blocker with an additional central serotonin 1A (5HT1A) receptor agonistic effect, for 12 weeks. Plasma fibrinogen concentration decreased by 24% (P < .0001) during urapidil treatment and by 9% (P = .05) during atenolol treatment, with the effects of the two drugs differing significantly. Plasminogen activator inhibitor (PAI) activity tended to increase by 17% (nonsignificant [NS]) in the atenolol-treated group and to decrease by 4% (NS) in the urapidil group. Differences between the effects of the two drugs on very-low-density lipoprotein (VLDL) triglycerides (TG) and on total TG were significant. During urapidil medication, these two parameters were reduced by 22% and 13%, respectively, but the changes were nonsignificant (P = .11 and P = .14, respectively). In contrast, atenolol treatment caused a significant increase in both VLDL TG and total TG of 31% and 21%, respectively. Hemoglobin A1c (HbA1c) increased by 4% (P = .06) during atenolol treatment, but was unaffected by urapidil. There were no significant changes within or between atenolol- and urapidil-treated groups regarding glucose disposal on an oral glucose tolerance test (OGTT) or the insulin sensitivity index on a hyperinsulinemic-euglycemic clamp test. In conclusion, urapidil treatment was characterized by neutral or favorable effects on several variables associated with the metabolic syndrome. Atenolol treatment had neutral properties in some metabolic aspects, but deleterious effects on lipid status.
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PMID:Urapidil treatment decreases plasma fibrinogen concentration in essential hypertension. 884 76


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