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

To investigate the metabolic effects of medroxyprogesterone acetate, carbohydrate and lipid metabolism in women with polycystic ovary syndrome was evaluated before and after long-term therapy with this drug. The effects of suppression of pituitary gonadotropins and ovarian sex steroids were correlated with the response to an oral glucose load and with a serum lipid profile. Twenty of 25 women with polycystic ovary syndrome weighted more than 150% of their ideal body weight. None of the patients had fasting hyperglycemia. Fasting and peak serum insulin responses to glucose were abnormally high in most patients with polycystic ovary syndrome. Fasting serum insulin had a significant positive correlation with percent ideal body weight (r = .7, P less than .01). High density lipoprotein cholesterol was low in all patients studied, whereas total cholesterol and serum triglyceride levels were normal. Therapy with medroxyprogesterone acetate did not affect body weight, glucose tolerance, or serum lipids. The correlations between serum testosterone and high-density lipoprotein cholesterol or insulin levels were not significant (P greater than .1). The authors conclude that medroxyprogesterone acetate does not affect the metabolic syndrome of obesity, hyperinsulinemia, and decreased high-density lipoprotein cholesterol that is commonly seen in patients with polycystic ovary syndrome.
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PMID:Abnormalities of fuel metabolism in the polycystic ovary syndrome. 621 33

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis]. 772 46

Type IIB muscle fibres are among the most insulin-insensitive muscle fibres and are not adapted to oxidation of fat during muscle work. The first characteristic of this type of muscle fibre most probably reflects or contributes to further development of insulin resistance contribute to further perpetuation of obesity and to the channeling of excess free fatty acids to the liver followed by secondary deterioration of its function. The impaired functioning of the liver is epitomized, among other changes, by impairment of insulin extraction. The increasing hyperinsulinaemia is followed by inhibition of synthesis of specific proteins such as carrier proteins for transporting testosterone (sex hormone binding globulin, SHBG). This results in an increased free testosterone concentration which induces androgenization in women and may further increase insulin insensitivity in abdominal obesity in women. The poor capillarization and changed muscle morphology in spite of great interindividual variety is observed in several pathological conditions characterised by insulin sensitivity (stroke, PCO, hypertension, diabetes, obesity). It is suggested that, in addition to the previous concept of the main role of intraabdominal adipose tissue, even muscles and liver are also important organs contributing to the pathogenesis and development of the metabolic syndrome.
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PMID:Role of muscle morphology in the development of insulin resistance and metabolic syndrome. 783 Dec 32

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

Recent evidence suggests that insulin is mitogenic on the adrenal cortex and stimulates adrenocortical tumor formation. We, investigated whether hyperinsulinemia is present in 13 patients with incidentally detected adrenal tumors. Patients with adrenal incidentalomas were obese (mean BMI 29.7 +/- 1.2 kg/m2, normal < 25; % body fat 35 +/- 1.5%, normal < 30%) with increased abdominal fat deposition (waist to hip ratio 0.92 +/- 0.02, normal < 0.85). All 13 patients were insulin resistant. Five had NIDDM, of the remaining patients 5 had fasting insulin concentrations above 15 microE/ml, and all 8 patients had elevated insulin concentrations after 75 g of glucose orally. To further investigate the potential role of insulin we examined its effects on the NCI-h295 cell line. Insulin (1-100 micrograms/ml) stimulated cell proliferation in a time and dose-dependent matter without affecting cortisol synthesis. At this concentrations insulin was equally potent to IGF I (10-80 ng/ml) or IGF II (10-100 ng/ml). We conclude that the majority of patients with adrenal incidentalomas are insulin-resistant/hyperinsulinemic. Insulin stimulates adrenal cancer cell lines in vitro. We propose that adrenal incidentalomas are a newly recognized manifestation of the metabolic syndrome comparable to insulin-mediated stimulation of the ovary in the polycystic ovary syndrome.
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PMID:Adrenal incidentalomas: a manifestation of the metabolic syndrome? 896 38

Recently, an inverse correlation between serum uric acid concentrations and insulin sensitivity has been described in subjects with varying degrees of metabolic syndrome, suggesting that measurement of serum uric acid may provide a simple marker of insulin resistance. Several biochemical and clinical features of polycystic ovary syndrome (PCOS) resemble those of metabolic syndrome: women with PCOS are often obese; they are also at increased risk for the development of coronary artery disease, hypertension and diabetes mellitus. The objective of the present study was to analyse the usefulness of serum uric acid measurement in screening for the metabolic syndrome in women with PCOS. For that purpose serum concentrations of uric acid, insulin and triglycerides were measured in 38 women with PCOS and 20 weight-matched control women with regular menstrual cycles. No differences were found in the uric acid concentrations between the PCOS and control groups. The mean concentrations of triglycerides and fasting insulin were higher in the women with PCOS than in the healthy controls. Serum uric acid concentrations were inversely related to serum hormone-binding globulin (SHBG) concentrations, and positively with body mass index (BMI), insulin concentrations and testosterone:SHBG ratio in the PCOS group. Our results suggest that measurement of serum uric acid does not provide new means for identification of metabolic syndrome in patients with PCOS.
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PMID:Normal serum uric acid concentrations in women with polycystic ovary syndrome. 898 Nov 20

We recently reported the frequent occurrence of polycystic ovaries and hyperandrogenism associated with weight gain and hyperinsulinemia in women taking valproate for epilepsy. The purpose of this study was to evaluate the risks related to valproate-induced hyperinsulinemia and their reversibility after discontinuing the medication. Sixteen women with valproate-related polycystic ovaries or hyperandrogenism participated in the study. Vaginal ultrasonography was performed, and endocrine and lipid parameters were measured. Thereafter, lamotrigine was substituted for valproate and the patients were observed for 12 months. Twenty-four healthy age-matched women served as control subjects. Twelve women completed the 12-month follow-up. While still on valproate they had centripetal obesity with associated hyperinsulinemia and unfavorable serum lipid profiles. The body-mass index and fasting serum insulin and testosterone concentrations decreased during the first year after replacing valproate with lamotrigine whereas the HDL-cholesterol/total cholesterol ratios increased from 0.17 +/- 0.06 to 0.26 +/- 0.05. The total number of polycystic ovaries in these women decreased from 20 during valproate medication to 11 one year after replacing valproate with lamotrigine. Valproate induces a metabolic syndrome with centripetal obesity, hyperinsulinemia, lipid abnormalities, and polycystic ovaries/hyperandrogenism in women with epilepsy. These valproate-related risks can be reduced by substituting lamotrigine for valproate.
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PMID:Valproate, lamotrigine, and insulin-mediated risks in women with epilepsy. 954 24

According to the actual knowledge obesity is a serious, nutrition-dependent pathology with a high number of consequences. Endocrine sequence of obesity such as PCO-HAIR-syndrome (polycystic ovarian syndrome, hyperandrogenemia-insulin-resistance) with its cycle disorders and sterility are beginning already in adolescent and women of young reproductive age. With ageing more serious risks such as non-insulin dependent diabetes mellitus (NIDDM), arteriosclerosis followed by coronary disease, stroke and hypertension, metabolic syndrome and a higher prevalence of malignant diseases will appear. Based on these five risks obesity should be treated early when therapeutic strategies are more successful than in older ages. The definition of a diagnosis and the beginning of a weight reduction programme combined with intense motivating treatment as well as medical and psychotherapeutic guidance is an important preventive contribution.
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PMID:[Obesity--significance in adolescence and for reproduction]. 962 28

Obesity gains increasing prevalence world-wide. Multifactorially caused it presents itself in numerous heterogeneous phenotypes with a wide spectrum of clinical symptoms. The full-blown female obesity syndrome is initiated already in childhood, associated with ovarian hyperandrogenaemia (polycystic ovary syndrome) in the reproductive phase, and characterised by increasing co-morbidity (cancer; metabolic syndrome; arteriosclerosis) in the postmenopausal state leading to shortened longevity. Due to the complexity of psychic, somatic and endocrine-metabolic disturbances a causal break-through in the treatment of the disease could not be achieved yet, but the enhanced basal understanding and recently investigated pharmaceutical principles might enable to improve the therapeutical approaches.
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PMID:Obesity in female life--from molecular to clinical aspects. 962 29

Obesity may either be unspecific as indicated by an increased body mass index (BMI) or due to an abnormal fat-distribution as indicated by an increased waist-to-hip ratio (WHR). The latter is frequently associated with deteriorations of glucose tolerance, hypertriglyceridaemia and hypertension (the metabolic syndrome), a syndrome which is among the strongest risk factors of ischemic heart disease. It is important to note that visceral obesity is a frequent feature of the polycystic ovary syndrome. Also, weight gain after menopause is often associated with a particular increase of the WHR. Obesity as indicated by an increased BMI (> 30 kg/m2) is a weak but easily detectable risk marker of venous thrombotic disease. This risk needs to be considered in clinical practice since obesity was shown to enhance the power of precipitating risk factors of venous disease such as pregnancy, surgery or estrogen treatment.
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PMID:[Obesity and thrombotic vascular diseases]. 962 33


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