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

Metabolic syndrome is a cluster of metabolic abnormalities consisting essentially of obesity, especially abdominal obesity. Metabolic syndrome has been highlighted as a risk factor for cardiovascular and other chronic diseases. Obesity has been implicated in various gastrointestinal diseases such as gastroesophageal reflux diseases and colorectal cancer. Recently, abdominal obesity has been shown to be more important than obesity as expressed by an elevated body mass index as a causative factor for the development of these diseases. In addition to the mechanical effects of obesity, such as an increase in intra-abdominal pressure from large amounts of adipose tissue, substances that adipose tissues secrete, such as tumor necrosis factor-alpha, interleukin-6, leptin, and insulin-like growth factor-1, have been proposed to be pathogenic links to these diseases. In this review, we discuss the association of metabolic syndrome or the individual components of metabolic syndrome, focusing on obesity and abdominal obesity, with gastrointestinal diseases.
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PMID:Metabolic syndrome and gastrointestinal diseases. 1746 54

Just as the blood-brain barrier (BBB) is not a static barrier, the adipocytes are not inert storage depots. Adipokines are peptides or polypeptides produced by white adipose tissue; they play important roles in normal physiology as well as in the metabolic syndrome. Adipokines secreted into the circulation can interact with the BBB and exert potent CNS effects. The specific transport systems for two important adipokines, leptin and tumor necrosis factor alpha, have been characterized during the past decade. By contrast, transforming growth factor beta-1 and adiponectin do not show specific permeation across the BBB, but modulate endothelial functions. Still others, like interleukin-6, may reach the brain but are rapidly degraded. This review summarizes current knowledge and recent findings of the rapidly growing family of adipokines and their interactions with the BBB.
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PMID:Adipokines and the blood-brain barrier. 1754 Apr 80

HIV-associated lipodystrophy or lipoatrophy, unreported before the introduction of highly active antiretroviral therapy (HAART), was first described in 1998, and has a prevalence ranging from 18% to 83%. As in genetic lipodystrophy syndromes, fat redistribution may precede the development of metabolic complications (dyslipidemia, insulin resistance) in HIV-infected patients receiving HAART. The pathogenesis of HAART-associated lipodystrophy and metabolic syndrome is complex and a number of factors are involved, including direct effects of HAART on lipid metabolism, endothelial and adipocyte cell function, and mitochondria. Protease inhibitors are responsible for a decrease in cytoplasmic retinoic-acid protein-1, in low density lipoprotein-receptor-related protein and in peroxisome proliferator activated receptor type-gamma. Nucleoside reverse transcriptase inhibitors, and thymidine analogues, are responsible for mitochondrial dysfunction as demonstrated by a decrease in subcutaneous adipose tissue mitochondrial DNA content. Both phenomena are responsible for a decreased differentiation of adipocytes, increased levels of free fatty acids and lipoatrophy. The increased levels of proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin-6 may further contribute in development of lipodystrophy. TNF-alfa activates 11-beta-hydroxysteroid dehydrogenase type-1, which converts inactive cortisone to active cortisol, resulting in increased lipid accumulation in adipocytes and insulin resistance. HAART drugs and inflammatory cytokines are associated with a decrease in adiponectin. The levels of adiponectin and adiponectin-to-leptin ratio correlate positively with insulin resistance in HIV-infected patients with lipodystrophy. HAART-associated metabolic syndrome is an increasingly recognized clinical entity. The atherogenic profile of this syndrome may increase the risk of cardiovascular disease even in young HIV-infected patients. A better understanding of the molecular mechanisms responsible for this syndrome will lead to the discovery of new drugs that will reduce the incidence of lipodystrophy and related metabolic complications in HIV-infected patients receiving HAART.
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PMID:Visceral fat as target of highly active antiretroviral therapy-associated metabolic syndrome. 1762 54

We investigated the determinants of endothelial function in 100 asymptomatic, non-diabetic, non-smokers with and without the metabolic syndrome ((MS)--defined by ATP-III criteria). Subjects with MS (n=24) had greater endothelial dysfunction (ED, P<0.001) than subjects without MS. One-way analysis of variance demonstrated a significant negative linear trend between level of ED (F=21.89; P<0.001) and number of ATP-III metabolic diagnostic criteria present in each subject. In a stepwise multivariate logistic regression model presence/absence of MS was the only independent determinant of ED (P=0.01). Age, gender, LDL cholesterol, C-reactive protein, interleukin-6 and tumour necrosis factor-alpha receptor 2 had no independent influence on endothelial function. In the absence of MS as variable there was no independent association between the remaining variables and endothelial function. Receiver operating characteristic (ROC) curves demonstrated that a combination of age, LDL cholesterol and CRP levels and presence/absence of MS can be used to predict ED (area under curve 0.81+/-0.06) and thus potentially may be used as a simple screening test to identify subjects with the greatest level of ED (sensitivity=0.82, specificity=0.72). Our study demonstrated that subjects with MS had greater ED. The extent of ED increased with presence of each additional ATP-III diagnostic criteria. Presence/absence of MS was the only independent predictor of ED and in conjunction with age, LDL cholesterol and CRP levels could be used as a potential simple clinical screening test for ED.
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PMID:Determinants of endothelial function in asymptomatic subjects with and without the metabolic syndrome. 1765 41

The objective of this study was to assess the capacity of different criteria of metabolic syndrome (MetS) to identify risks of coronary heart diseases (CHDs) and related changes of adipocytokines in postmenopausal women. A cross-sectional study was carried out in 225 community-dwelling, elderly postmenopausal Chinese women (age, 66.77+/-5.09 years) without hormone replacement therapy (HRT). Baseline data such as blood pressure, body mass index (BMI), serum lipid profiles, and fasting glucose were analyzed, and insulin sensitivity was estimated via the homeostasis model assessment for insulin resistance. Serum tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), and adiponectin were measured simultaneously. The prevalence of MetS identified by the Third Report of the National Cholesterol Education Programme Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, the International Diabetes Federation (IDF), the Chinese Diabetes Society (CDS), and the Japanese Society of Internal Medicine (JPN) were 27.31%, 37.34%, 23.29%, and 13.65%, respectively. No significant differences of baseline data were found among different MetS groups, except for a significant higher waist circumference in the JPN-MetS group as compared with other MetS groups. The prevalence of confirmed CHD in the four MetS groups were 26.2%, 18.6%, 26.9%, and 32%, respectively. Odds ratios for CHD were 1.905 (95% CI=1.273-2.851), 1.208 (95% CI=0.778-1.876), 1.997 (95% CI=1.238-3.221), and 2.336 (95% CI=1.119-4.876), respectively. The JPN-MetS group had higher levels of TNFalpha and IL-6, whereas the CDS-MetS group correlated better with lower adiponectin levels. The IDF definition for MetS is the most sensitive one with regard to metabolic disorders, whereas JPN and CDS definitions correlate better with CHD and changes of adipocytokines among the four criteria studied.
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PMID:Risks of CHD identified by different criteria of metabolic syndrome and related changes of adipocytokines in elderly postmenopausal women. 1782 56

We investigated in a young Italian obese population, the relationship between ambulatory BP (ABP) and several pathophysiological factors linking obesity to hypertension. A total of 89 obese children and adolescents underwent a 24-h ambulatory BP monitoring (ABPM) and an oral glucose tolerance test. The circulating levels of insulin, lipids, uric acid, C-reactive protein, interleukin-6, renin and aldosterone and the 24-h urinary levels of epinephrine, norepinephrine and albumin excretion rate were measured. Nine percent of subjects had daytime sustained hypertension (SH), 26% night-time hypertension and 11% a non-dipping pattern. SH subjects compared to those with sustained normotension (SN) were more obese (P<0.05), with a more frequent family history of hypertension (P<0.05), higher urinary catecholamine (P<0.05) and heart rate values (P<0.05) after adjustment for standard deviation score (SDS) of body mass index (BMI) and sex. Subjects with night-time hypertension compared to those with night-time normotension were more obese (P<0.0001), with a higher prevalence of impaired glucose tolerance (P<0.05) and metabolic syndrome (P<0.05) and higher 2-h glucose (P<0.05), uric acid (P<0.05) and triglycerides (P<0.05). In multivariate regression analysis, daytime systolic BP (SBP) remained independently correlated with urinary norepinephrine and SDS-BMI (P<0.05 for both), daytime diastolic BP (DBP) with waist circumference (P<0.05) and night-time SBP and DBP with SDS-BMI (P<0.01 for both). The risk of having systolic and diastolic hypertension increased with the increase in SDS-BMI and waist circumference, respectively. In conclusion, in our cohort of obese children and adolescents, daytime and night-time hypertension were associated with activation of the sympathoadrenal system and worst metabolic conditions, respectively.
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PMID:Sympathoadrenergic and metabolic factors are involved in ambulatory blood pressure rise in childhood obesity. 1788 27

Metabolic syndrome and type 2 diabetes (T2DM) resulting from sustained hyperglycemia are considered as risk factors for cardiovascular disease (CVD) but the mechanism for their contribution to cardiopathogenesis is not well understood. Hyperglycemia induces nonenzymatic glycation of protein-yielding advanced glycation end products (AGE), which are postulated to stimulate interleukin-6 (IL-6) expression, triggering the liver to secrete tissue necrosis factor alpha (TNF-alpha) and C-reactive protein (CRP) that contribute to CVD pathogenesis. Although the high prevalence of periodontitis among individuals with diabetes is well known by dental researchers, it is relatively unrecognized in the medical community. The expression of the same proinflammatory mediators implicated in hyperglycemia (i.e., IL-6, TNF-alpha, and CRP) have been reported to be associated with periodontal disease and increased risk for CVD. We will review published evidence related to these 2 pathways and offer a consensus.
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PMID:Oral infection, hyperglycemia, and endothelial dysfunction. 1790 6

The metabolic syndrome (MetS), characterized by a clustering of cardiovascular disease and type 2 diabetes (T2DM) risk factors, has become prevalent in children and adolescents in recent years. However, the reported prevalence data on the MetS in youths has varied markedly, in large part, because of the disagreement among the variously proposed definitions of the MetS. Obesity is defined by using body mass index, waist circumference, or percent overweight, pointing to the need for standardized use of anthropometric variables to define obesity with a well-defined reference year for each ethnic population. In addition, slightly different cutoff values are used for triglycerides, high-density lipoprotein cholesterol, blood pressure, and fasting plasma glucose. Therefore, International Diabetes Federation recently proposed unified, easy-to-use criteria for diagnosing the MetS in youths. To provide insight into the mechanisms underlying the MetS in youths, the degree of insulin sensitivity/resistance and its correlation with the serum lipid and blood pressure levels have been evaluated. In addition, the serum levels of adipocytokines, such as adiponectin, leptin, tumor necrosis factor-alpha, resistin, interleukin-6, plasminogen activator inhibitor-1, and their correlation with childhood obesity have been extensively investigated. Recommendations for future research include exploring ways to assess visceral adiposity, to identify better biochemical markers for prediction of T2DM and disease progression, and to effectively intervene to prevent the MetS in youths.
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PMID:Metabolic syndrome in youths. 1799 Nov 33

Adipose tissue inflammation and insulin resistance are central to the pathogenesis of the metabolic syndrome. Spironolactone, an antagonist of mineralocorticoid receptor, glucocorticoid receptor and androgen receptor, and agonist of progesterone receptor, has anti-inflammatory activity. Blockade of the renin-angiotensin-aldosterone system has been shown to improve glucose metabolism. We have investigated whether spironolactone has direct effects on glucose uptake and interleukin-6 secretion in human adipocytes. Spironolactone, but not its active metabolite canrenoic acid, significantly increased basal and insulin-stimulated glucose uptake in cultured IN VITRO-differentiated adipocytes of women, without affecting insulin sensitivity. The effect was not due to changes in abundance of glucose transporters 1 or 4 or in degree of cell differentiation. Spironolactone, but not canrenoic acid, significantly reduced basal interleukin-6 secretion by cultured stromal-vascular cells. These effects of spironolactone were not mediated by ligand-dependent antagonism of the mineralocorticoid, glucocorticoid, or androgen receptors. Spironolactone may have a novel role in increasing glucose uptake into adipose cells and attenuating adipose tissue inflammation, with implications for management of metabolic syndrome.
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PMID:Effects of spironolactone on glucose transport and interleukin-6 secretion in adipose cells of women. 1807 71

Derangements in whole body glucose and lipid metabolism, accompanied by insulin resistance, are key features of obesity and the metabolic syndrome. A role for inflammation as a causative factor is an emerging concept in the field of metabolic disease. Research has centred on identifying important inflammatory markers, and tumour necrosis factor-alpha has been highlighted as a key mediator of insulin resistance, as well as interleukin-6 (IL-6). A parallel ongoing endeavour is the unravelling of molecular mechanisms underlying the beneficial effects of physical exercise on whole body glucose and lipid metabolism. Release of IL-6 from the contracting skeletal muscle has been proposed to be one of the molecular signals promoting the beneficial exercise-induced effects. These two opposing views of IL-6 underscore that the role of IL-6 in whole body physiology is incompletely resolved. This review aims at summarizing the current data on mechanisms by which IL-6 may impact on glucose and lipid metabolism.
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PMID:Role of interleukin-6 signalling in glucose and lipid metabolism. 1817 28


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