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

The authors present the history of selecting and understanding the essence of the metabolic syndrome (X syndrome, Reaven's syndrome) related to insulin resistance as well as its contemporary working definition allowing diagnosing affected individuals. They describe the cycle of their own study investigating the prevalence of metabolic syndrome elements in patients treated because of their thyrotoxicosis. It has been observed that 4 weeks after thyrostatic treatment is started, many of these patients are affected by the growth of their body mass and total cholesterol level (mostly at the cost of LDL-cholesterol). After 2 years the growth of body mass is significant, many patients develop arterial hypertension. After 15 years of obesity, diabetes type 2 (DM-2), arterial hypertension, dyslipidemia, hyperinsulinaemia and full metabolic syndrome are found much more frequently than in the control group. In the research carried in the 1987--1989 period, we found the following in 11,546 subjects from the Lublin region (villagers aged over 18): overweight in 36% women and 34% of men, and obesity in 30% of women and 10% of men, and arterial hypertension in 24.2% and DM 2 in 2.7% of the whole examined group. Within the research carried out between 1998 and 2000 we examined 3,782 persons (63%) out of 6,000 persons aged over 35 carefully selected from the Lublin town and the Lublin region villages. DM 2 was found in 17.6% of the examined in the countryside and in 14.1% from the town (newly diagnosed diabetes--75% and 56% respectively). Obesity (BMI > or = 30 kg/m2) was found in 30.8% of the examined from villages and 30.1% town dwellers, arterial hypertension (RR > or = 140/90 mmHg) was found in 69.4% villagers and 68.6% subjects from the town. Total serum cholesterol > or = 5.2 mmol/l (200 mg/dl) was found in 66.4% of the examined from the countryside and in 60% from the town, LDL-cholesterol > or = 3.5 mmol/l (135 mg/dl) was found in 57.3% and 52.6% respectively, and triglycerides > or = 1.7 mmol/l (150 mg/dl) in 33,3% and 44.8 respectively. Hypo-HDL-cholesterolaemia was found in 21.7% of the examined from villages and in 31.4% of the examined from Lublin. 76.5% of the examined from the countryside and 72.7% from the town had a raised WHR index.
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PMID:Metabolic syndrome. 1531 27

Adiponectin is one of the most thoroughly studied adipocytokines. Low plasma levels of adiponectin are found to associate with obesity, metabolic syndrome, diabetes and many other human diseases. From animal experiments and human studies, adiponectin has been shown to be a key regulator of insulin sensitivity. In this article, we review the evidence and propose that hypo-adiponectinemia is not a major cause of obesity. Instead, it is the result of obesity-induced insulin resistance in the adipose tissue. Hypo-adiponectinemia then mediates the metabolic effects of obesity on the other peripheral tissues, such as liver and skeletal muscle and may also exert some direct effects on end-organ damage. We propose that deciphering the molecular details governing the adiponectin gene expression and protein secretion will lead us to more comprehensive understanding of the mechanisms of insulin resistance in the adipose tissue and provide us new avenues for the therapeutic intervention of obesity and insulin resistance-related human disorders.
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PMID:Adiponectin: a biomarker of obesity-induced insulin resistance in adipose tissue and beyond. 1853 23

Metabolic syndrome (MetS) includes some parameters which are associated with cardiovascular events and risk of developing heart failure (HF). The aim of the present study was to explore the prevalence of metabolic syndrome and individual MetS parameters among heart failure patients. Stable HF patients who had an ejection fraction (EF) < or = 35% were included. They were evaluated for MetS and parameters according to the Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program (NCEP). One hundred and nine patients (72 males, 37 females; mean age, 67 +/- 12 years) were included. The most prevalent parameters were low HDL-C (69%) and hypertension (69%) in all participants. No significant change was observed in the prevalence of these parameters due to gender (P > 0.05). Hypertension, increased waist circumference, and hypertriglyceridemia were all significantly more common in women (P < 0.05). The prevalences of hypo-HDL-emia, hyperglycemia, and hypertension did not differ significantly with an advanced age (P > 0.05), whereas hypertriglyceridemia and high waist circumference were significantly decreased in the elderly (P < 0 05). The overall MetS prevalence was 51% and it was significantly higher in women (76% versus 37%, P : 0.003). The prevalence of MetS clearly decreased with age, although the difference was not statistically significant (61% versus 46%, P : 0.57). The mean number of positive MetS parameters also changed significantly with age (3 +/- 1.4 versus 2.5 +/- 1.3, P : 0.046). EF did not change with mean number of MetS parameters (P > 0.05). Hypo-HDL-emia and similarly hypertension were the 2 most common MetS parameters in HF patients. Hypo-HDL-emia and hypertension were the most common parameters observed in all participants and no significant difference was seen due to gender or age. Even though the prevalence of MetS and the mean number of parameters were significantly more common in females and young patients, EF did not change with changes in these parameters. Based on the results obtained, we conclude that the early diagnosis and treatment of MetS as well as the measurement of individual parameters, especially the most frequent ones, may prevent heart failure or improve its status.
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PMID:Low HDL levels as the most common metabolic syndrome risk factor in heart failure. 1980 6

Epidemiological studies estimate that greater than 60% of the adult US population may be categorized as either overweight or obese, and there is a growing appreciation that the complications of obesity extend to the central nervous system (CNS). While the vast majority of these studies have focused on the hypothalamus, more recent studies suggest that the complications of obesity may also affect the structural and functional integrity of the hippocampus. A potential contributor to obesity-related CNS abnormalities is the adipocyte-derived hormone leptin. In this regard, decreases in CNS leptin activity may contribute to deficits in hippocampal synaptic plasticity and suggest that leptin resistance, a well-described phenomenon in the hypothalamus, may also be observed in the hippocampus. Unfortunately, the myriad of metabolic and endocrine abnormalities in diabetes/obesity phenotypes makes it challenging to assess the role of leptin in hippocampal neuroplasticity deficits associated with obesity models. To address this question, we examined hippocampal morphological and behavioral plasticity following lentivirus-mediated downregulation of hypothalamic insulin receptors (hypo-IRAS). Hypo-IRAS rats exhibit increases in body weight, adiposity, plasma leptin and triglyceride levels. As such, hypo-IRAS rats develop a phenotype that is consistent with features of the metabolic syndrome. In addition, hippocampal morphological plasticity and performance of hippocampal-dependent tasks are adversely affected in hypo-IRAS rats. Leptin-mediated signaling is also decreased in hypo-IRAS rats. We will discuss these findings in the context of how hyperleptinemia and hypertriglyceridemia may represent mechanistic mediators of the neurological consequences of impaired hippocampal synaptic plasticity in obesity.
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PMID:Obesity/hyperleptinemic phenotype impairs structural and functional plasticity in the rat hippocampus. 2135 91

Ongoing epidemiological studies estimate that greater than 60% of the adult US population may be categorized as either overweight or obese. There is a growing appreciation that the complications of obesity extend to the central nervous system (CNS) and may result in increased risk for neurological co-morbidities like depressive illness. One potential mechanistic mediator linking obesity and depressive illness is the adipocyte derived hormone leptin. We previously demonstrated that lentivirus-mediated downregulation of hypothalamic insulin receptors increases body weight, adiposity and plasma leptin levels, which is consistent with features of the metabolic syndrome. Using this novel model of obesity, we examined performance in the forced swim test (FST), the sucrose preference test and the elevated plus maze (EPM), approaches that are often used as measures of depressive-like and anxiety-like behaviors, in rats that received third ventricular injections of either an insulin receptor antisense lentivirus (hypo-IRAS) or a control lentivirus (hypo-Con). Hypo-IRAS rats exhibited significant increases in immobility time and corresponding decreases in active behaviors in the FST and exhibited anhedonia as measured by decreased sucrose intake compared to hypo-Con rats. Hypo-IRAS rats also exhibited increases in anxiety-like behaviors in the EPM. Plasma, hippocampal and amygdalar brain-derived neurotrophic factor (BDNF) levels were reduced in hypo-IRAS rats, suggesting that the obesity/hyperleptinemic phenotype may elicit this behavioral phenotype through modulation of neurotrophic factor expression. Collectively, these data support the hypothesis for an increased risk for mood disorders in obesity, which may be related to decreased expression of hippocampal and amygdalar BDNF.
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PMID:Downregulation of hypothalamic insulin receptor expression elicits depressive-like behaviors in rats. 2145 99

Microparticles are membrane vesicles with pro-inflammatory properties. Circulating levels of microparticles have previously been found to be elevated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the effects of in vivo treatment with microparticles, from patients with MetS and from healthy subjects (HS), on ex vivo vascular function in mice. Microparticles isolated from MetS patients or HS, or a vehicle were intravenously injected into mice, following which vascular reactivity in response to vasoconstrictor agonists was assessed by myography with respect to cyclo-oxygenase pathway, oxidative and nitrosative stress. Injection of microparticles from MetS patients into mice induced vascular hypo-reactivity in response to serotonin. Hypo-reactivity was associated with up-regulation of inducible NO-synthase and increased production of NO, and was reversed by the NO-synthase inhibitor (N(G)-nitro-L-arginine). The selective COX-2 inhibitor (NS398) reduced the contractile effect of serotonin in aortas from mice treated with vehicle or HS microparticles; however, this was not observed within mice treated with MetS microparticles, probably due to the ability of MetS microparticles to enhance prostacyclin. MetS microparticle-mediated vascular dysfunction was associated with increased reactive oxygen species (ROS) and enhanced expression of the NADPH oxidase subunits. Neutralization of the pro-inflammatory pathway Fas/FasL completely prevented vascular hypo-reactivity and the ability of MetS microparticles to enhance both inducible NO-synthase and monocyte chemoattractant protein-1 (MCP-1). Our data provide evidence that microparticles from MetS patients induce ex vivo vascular dysfunction by increasing both ROS and NO release and by altering cyclo-oxygenase metabolites and MCP-1 through the Fas/FasL pathway.
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PMID:Microparticles from patients with metabolic syndrome induce vascular hypo-reactivity via Fas/Fas-ligand pathway in mice. 2211 Jul 64

The liver and its pleotropic functions play a fundamental role in regulating metabolism, and is also an inevitable target of multiple metabolic disorders. The numerous and constant relationships and feedback mechanisms between the liver and all endocrine organs is reflected by the fact that an alteration of one oftentimes results in the malfunction of the other. Hypo- and hyperthyroidism are frequently associated with hepatic alterations, and thyroid diseases must be excluded in transaminase elevation of unknown cause. Drugs such as propylthiouracil, used in the treatment of hyperthyroidism, may induce liver damage, and other drugs such as amiodarone, carbamazepine, and several chemotherapeutic agents can lead to both thyroid and liver abnormalities. Liver diseases such as hepatitis, hepatocellular carcinoma, and cirrhosis may cause altered levels of thyroid hormones, and alcoholic liver disease, both due to the noxious substance ethanol as well as to the hepatic damage it causes, may be responsible for altered thyroid function. Both excess and insufficiency of adrenal function may result in altered liver function, and adrenocortical dysfunction may be present in patients with cirrhosis, especially during episodes of decompensation. Again an important player which affects both the endocrine system and the liver, alcohol may be associated with pseudo-Cushing syndrome. Sex hormones, both intrinsic as well as extrinsically administered, have an important impact on liver function. While oestrogens are related to cholestatic liver damage, androgens are the culprit of adenomas and hepatocellular carcinoma, among others. Chronic liver disease, on the other hand, has profound repercussions on sex hormone metabolism, inducing feminization in men and infertility and amenorrhoea in women. Lastly, metabolic syndrome, the pandemia of the present and future centuries, links the spectrum of liver damage ranging from steatosis to cirrhosis, to the array of endocrine alterations that are features of the syndrome, including insulin resistance, central obesity, and hyperlipidaemia. Clinical practice must integrally evaluate the effects of the intricate and tight relationship between the liver and the endocrine system, in order to better address all manifestations, complications, and prevent deterioration of one or the other organ-system.
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PMID:Liver abnormalities and endocrine diseases. 2409 Sep 42

Metabolic syndrome (MetS) and thyroid dysfunction are common in clinical practice. The objectives of this review are to discuss some proposed mechanisms by which thyroid dysfunctions may lead to MetS, to describe the bidirectional relationship between thyroid hormones (THs) and adiposity and finally, to resume a list of recent studies in humans that evaluated possible associations between thyroid hormone status and MetS or its clinical components. Not solely THs, but also its metabolites regulate metabolic rate, influencing adiposity. The mechanisms enrolled are related to its direct effect on adenosine triphosphate (ATP) utilization, uncoupling synthesis of ATP, mitochondrial biogenesis, and its inotropic and chronotropic effects. THs also act controlling core body temperature, appetite, and sympathetic activity. In a bidirectional way, thyroid function is affected by adiposity. Leptin is one of the hallmarks, but the pro-inflammatory cytokines and also insulin resistance impact thyroid function and perhaps its structure. MetS development and weight gain have been positively associated with thyroid-stimulating hormone (TSH) in several studies. Adverse glucose metabolism may be related to hyperthyroidism, but also to reduction of thyroid function or higher serum TSH, as do abnormal serum triglyceride levels. Hypo- and hyperthyroidism have been related to higher blood pressure (BP), that may be consequence of genomic or nongenomic action of THs on the vasculature and in the heart. In summary, the interaction between THs and components of MetS is complex and not fully understood. More longitudinal studies controlling each of all confounding variables that interact with endpoints or exposure factors are still necessary.
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PMID:The role of thyroid hormone in metabolism and metabolic syndrome. 3248 80