Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with polycystic ovary syndrome (PCOS) have an increased prevalence of metabolic syndrome (MBS). Hypoadiponectinemia is closely associated with MBS. The aim of our study was to evaluate the association of adiponectin levels with MBS in patients with PCOS. We studied 60 patients with PCOS and 60 age-matched control subjects. Serum adiponectin, fasting glucose, triglycerides, high-density lipoprotein (HDL) levels, blood pressure and waist circumference were measured for each subject. The results showed that 33% of patients with PCOS were diagnosed with MBS; this was 11.7% in the control group (p<0.01). Adiponectin levels were significantly lower in PCOS patients with MBS than PCOS patients without MBS (p<0.001). After adjustment for body mass index (BMI), adiponectin levels were correlated negatively with waist circumference, triglycerides, diastolic blood pressure, homeostasis model assessment (HOMA) and positively with HDL. PCOS patients with adiponectin levels lower than median value had 10.5-fold higher risk of having MBS. Logistic regression analysis revealed that adiponectin levels were independently associated with the risk of having MBS, and the significance did not change after adjusting for each component of MBS. We concluded that patients with PCOS had an increased prevalence of MBS and thus an increased risk of cardiovascular disease. Hypoadiponectinemia was independently associated with MBS in these patients. Adiponectin as an endogenous biologically relevant modulator of vascular remodeling may have a role in the development of MBS in PCOS patients.
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PMID:Association of hypoadiponectinemia with metabolic syndrome in patients with polycystic ovary syndrome. 1827 10

This Finnish population-based study, mean age 46 years, evaluates the association of high-sensitivity C-reactive protein (hs-CRP), interleukin-1 receptor antagonist (IL-1Ra), and adiponectin with the NCEP and IDF definitions of metabolic syndrome (MetS). Adiponectin levels were higher, hs-CRP and IL-1Ra levels lower in subjects without MetS compared to subjects with MetS. If MetS was present according to both IDF and NCEP criteria, BMI, waist, triglycerides, hs-CRP, and IL-1Ra were significantly higher compared to subjects who had MetS according to either only IDF or only NCEP criteria. The hs-CRP, IL-1Ra, and adiponectin linearly correlated with the number of the components of MetS according to both definitions. Decreased levels of adiponectin and increased levels of hs-CRP and IL-1Ra are tightly associated with the components of MetS. Individuals who had MetS according to both criteria had the most adverse changes in cardiovascular risk factors.
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PMID:Association of C-reactive protein, interleukin-1 receptor antagonist and adiponectin with the metabolic syndrome. 1828 76

In Western culture, excess visceral fat accumulation or obesity has reached epidemic proportions, resulting in metabolic syndrome. However, more than 10 years of research has shown that adipocytes also function as endocrine cells that release various bioactive substances, so called "adipocytokines or adipokines", that play a major role in the regulation of food intake, insulin sensitivity, energy metabolism, and the vascular microenvironment. Adiponectin, an adipocytokine, is considered to improve insulin sensitivity. Recently, monocyte chemoattractant protein (MCP)-1 has been reported to be a novel adipocytokine involved in the development of obesity-associated insulin resistance and atherosclerosis. Nuclear receptors, especially peroxisome proliferator-activated receptor-alpha (PPAR alpha) and PPAR gamma are ligand-activated transcription factors that regulate the metabolism of glucose and lipids. PPAR gamma is strongly expressed in adipocytes and plays a significant role in the transcriptional activation of adipocytokines including adiponectin. PPAR alpha, another PPAR isoform, is involved in the control of lipid metabolism in the liver and skeletal muscle. PPAR alpha activation causes lipid clearance via beta-oxidation enhancement. We showed that various dietary terpenoids and other natural ingredients regulate the transcription of PPAR target genes, induces the expression and secretion of adiponectin, and inhibits those of MCP-1 in adipocytes and beta-oxidation in liver. These findings indicate that dietary factor acts as an agonist of PPARs and is a valuable medical and food component for the gradual improvement of metabolic syndrome.
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PMID:Dietary regulation of nuclear receptors in obesity-related metabolic syndrome. 1829 19

Adiponectin, an abundant adipocyte-derived plasma protein that modulates vascular function in type 2 diabetes, has been shown to provide cytoprotection to both pancreatic and vascular systems in diabetes. Therefore, we examined whether up-regulation of heme oxygenase (HO)-1 ameliorates the levels of inflammatory cytokines and influences serum adiponectin in Zucker fat (ZF) rats. ZF rats displayed a decrease in both HO activity and HO-1 and HO-2 protein levels and an increase in tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 compared with Zucker lean (ZL) rats. Treatment of ZF animals with 2 mg/kg cobalt protoporphyrin IX (CoPP) increased protein levels of HO-1 and HO activity, but HO-2 was unaffected. The increase in HO-1 was associated with a decrease in superoxide levels (p < 0.05) and an increase in plasma adiponectin (p < 0.005), compared with untreated ZF rats. CoPP treatment decreased visceral and s.c. fat content, and it reduced weight gain (p < 0.01). In addition, the inflammatory cytokines TNF-alpha and IL-6 were decreased (p < 0.04 and p < 0.008, respectively). Treatment of human bone marrow-derived adipocytes cultured with CoPP resulted in an increase in HO-1 and a decrease in superoxide levels. Up-regulation of HO-1 caused adipose remodeling, smaller adipocytes, and increased adiponectin secretion in the culture medium of human bone marrow-derived adipocytes. In summary, this study demonstrates that the antiobesity effect of HO-1 induction results in an increase in adiponectin secretion, in vivo and in vitro, a decrease in TNF-alpha and IL-6, and a reduction in weight gain. These findings highlight the pivotal role and symbiotic relationship of HO-1 and adiponectin in the modulation of the metabolic syndrome phenotype.
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PMID:Heme oxygenase-mediated increases in adiponectin decrease fat content and inflammatory cytokines tumor necrosis factor-alpha and interleukin-6 in Zucker rats and reduce adipogenesis in human mesenchymal stem cells. 1833 66

Studies performed during the last decade indicate that adipose tissue is not only a site of triglyceride storage but also an active endocrine organ which secretes many biologically active mediators referred to as "adipokines". In contrast to many adipokines which are overproduced in obese individuals and exert deleterious effects on insulin sensitivity, lipoprotein metabolism and cardiovascular system, such as leptin, tumor necrosis factor-alpha, plasminogen activator inhibitor-1, resistin, etc., adiponectin seems to be a unique adipokine which is produced in lower amounts in obese than in lean subjects and possesses predominantly beneficial activities, i.e. increases insulin sensitivity, stimulates fatty acid oxidation, inhibits inflammatory reaction and induces endothelium-dependent nitric oxide-mediated vasorelaxation. Adiponectin binds two receptors, AdipoR1 and AdipoR2. Adiponectin knockout mice exhibit various manifestations of the metabolic syndrome such as insulin resistance, glucose intolerance, hyperlipidemia, impaired endothelium-dependent vasorelaxation and hypertension, as well as augmented neointima formation after vascular injury. Clinical studies indicate that plasma adiponectin concentration is lower in patients with essential hypertension and ischemic heart disease. Raising endogenous adiponectin level or increasing the sensitivity to this hormone may be a promising therapeutic strategy for patients with metabolic and cardiovascular diseases. Among currently used drugs, thiazolidinediones (peroxisome proliferator activated receptor gamma agonists) are most effective in elevating adiponectin level.
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PMID:Adiponectin and its role in cardiovascular diseases. 1833 52

Adiponectin has potent insulin-sensitizing effects, improves lipid metabolism, and potentially protects against the development of metabolic syndrome. Thus, increasing adiponectin levels in preterm infants at risk for developing metabolic syndrome may be of special interest. The aim of this study was to examine the effects of dietary long-chain polyunsaturated fatty acids (LCPUFA) on serum adiponectin and lipid concentrations in preterm infants. Adiponectin and lipid levels of 60 healthy preterm infants [gestational age 32.7 (1.9) wk] randomly assigned to be fed either 1) a formula containing LCPUFA [arachidonic and docosahexanoic] (+LCPUFA group) or 2) the same formula without LCPUFA (-LCPUFA/control group), were determined at mean (SD) 33.8 (11.7) d. Adiponectin and HDL-C concentrations were significantly higher in the +LCPUFA group than in controls (p = 0.002 and p = 0.01, respectively); whereas, triglyceride levels were lower (p = 0.06). Adiponectin correlated positively with HDL-C levels and negatively with triglyceride levels in the +LCPUFA group but not in the controls. In conclusion, circulating adiponectin concentrations were higher in preterm infants fed a formula containing LCPUFA than infants fed an LCPUFA-free formula and they correlated with lipidemic profile.
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PMID:Circulating adiponectin in preterm infants fed long-chain polyunsaturated fatty acids (LCPUFA)-supplemented formula--a randomized controlled study. 1835 52

The metabolic syndrome (MS) is a clustering of cardiovascular risk factors, with insulin resistance as a major feature. This syndrome has been variously defined, but generally consists of 3 or more of the following components: hyperglycemia, hypertension, hypertriglyceridemia, low HDL, and increased abdominal circumference and/or BMI at >30 kg/m(2). The WHO criteria require the presence of insulin resistance to make the diagnosis. The current review focuses particularly on the association of the MS and the proinflammatory state as well as treatment options to prevent the development of coronary heart disease (CHD). Chronic inflammation is frequently associated with the MS. Inflammatory markers that have been associated with MS include hs-CRP, TNF-alpha, fibrinogen, and IL-6, among others. The link between inflammation and the MS is not fully understood. One postulated mechanism is that these cytokines are released into the circulation by adipose tissue, stimulating hepatic CRP production. The prothrombotic molecule PAI-1 is also increased in the MS. Adiponectin, produced exclusively by adipocytes, is decreased in obesity. The association of these proinflammatory and prothrombotic markers with the MS is discussed in detail. The general goals of treatment of the MS are prevention of CHD events and diabetes if not already present. The approach to treatment of those with the MS should include lifestyle changes, including weight loss and exercise as well as appropriate pharmacological therapies. Certain medications, which may be used in persons with MS, have been shown to have beneficial effects on clinical outcome and/or anti-inflammatory effects.
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PMID:The metabolic syndrome and inflammation. 1837 Jun 40

Adiponectin can suppress atherogenesis by inhibiting the adherence of monocytes, reducing their phagocytic activity, and suppressing the accumulation of modified lipoproteins in the vascular wall. Contradictory data have been reported about the effect of statins on adiponectin plasma levels. In this work, adiponectin plasma levels were measured in 102 statin-free subjects from the Spanish population of the Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (ACTFAST) study, a 12-week, prospective, multi-centre, open-label trial which enrolled subjects with coronary heart disease, coronary heart disease-equivalent or a 10-year coronary heart disease risk >20%. Subjects were assigned to atorvastatin (10-80 mg/day) based on low-density lipoprotein (LDL)-cholesterol concentration at screening. For comparison, age and gender-matched blood donors (N=40) were used as controls. Control subjects did not present hypertension, hypercholesterolemia, diabetes, metabolic syndrome and history of cardiovascular diseases. Adiponectin levels were diminished in patients at high cardiovascular risk compared with control subjects [4166 (3661-4740) vs 5806 (4764-7075) ng/ml respectively; geometric mean (95% CI); P<0.0001]. In the whole population, atorvastatin treatment increased adiponectin levels [9.7 (3.2-16.7);% Change (95% CI); P=0.003]. This increment was in a dose-dependent manner; maximal effect observed with atorvastatin 80 mg/d [24.7 (5.7-47.1); P=0.01]. Adiponectin concentrations were positively correlated with high-density lipoprotein-cholesterol both before and after atorvastatin treatment. No association was observed between adiponectin and LDL-cholesterol before and after atorvastatin treatment. In conclusion, atorvastatin increased adiponectin plasma levels in subjects at high cardiovascular risk, revealing a novel anti-inflammatory effect of this drug.
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PMID:Adiponectin plasma levels are increased by atorvastatin treatment in subjects at high cardiovascular risk. 1837 27

To determine the relative contribution of obesity and visceral white adipose tissue (WAT) to metabolic syndrome, we developed a model that is susceptible to high-fat diet-induced obesity and insulin resistance using male KK/Ta mice. The ratio of WAT weight to body weight was greater in the high-fat diet group compared with the control group in 10-, 14-, and 22-week-old mice. The increase in visceral WAT preceded development of fatty liver and insulin resistance. Adiponectin mRNA expression in WAT was markedly decreased before the decrease in its plasma levels or the development of insulin resistance. Insulin resistance appeared in association with fatty infiltration and TNF-alpha expression in the liver in 22-week-old mice. These data indicate that our mouse model would be useful for future studies that investigate the role of visceral WAT and its products in the development of metabolic syndrome.
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PMID:A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice. 1838 33

The authors compared postpartum adiponectin levels among women with prior pregnancy-induced disturbances and assessed their association with homeostasis model assessment for insulin resistance (HOMA-IR), the metabolic syndrome (MS), and the Framingham risk score (FRS). Women delivering in 1998 through 2001 and who had gestational diabetes mellitus (n=22), gestational hypertension (n=32), or preeclampsia (n=34) were examined 1 to 2 years after delivery and were grouped-matched to controls (n=29) by age and prepregnancy body mass index. HOMA-IR was increased, adiponectin values were decreased, and there was a higher MS prevalence in women with prior gestational diabetes mellitus (all P<.05). Adiponectin levels were inversely related to HOMA-IR (r=-0.45; P<.0001) and FRS (r=-0.25; P=.007), and a significant trend for decreasing adiponectin values with increased number of MS components was noted (P trend <.0001). Adiponectin concentration remained a significant correlate of FRS and MS irrespective of pregnancy history; a concentration <10.5 microg/mL provided the optimal cutoff to distinguish those with or without MS. Thus, a lower postpartum adiponectin concentration identifies women at increased cardiovascular risk regardless of pregnancy history.
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PMID:Postpartum adiponectin concentration, insulin resistance and metabolic abnormalities among women with pregnancy-induced disturbances. 1840 Dec 39


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