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)

This study was designed to investigate the possible beneficial effects of consuming a sodium-rich carbonated mineral water on lipoprotein metabolism and to determine whether consumption of this water influences endothelial dysfunction (ED) in postmenopausal women. Women included in the study were amenorrheic (>1 y), healthy, and not obese (BMI < 30 kg/m(2)). The subjects did not take estrogen replacement therapy; supplements of vitamins, minerals, and phytoestrogens; or other medications known to affect bone and lipid metabolism. The study consisted of 2 intervention periods of 2 mo each, during which women drank 1 L/d of a control mineral water (low mineral content) for 2 mo followed by the carbonated mineral water, rich in sodium, bicarbonate, and chloride, for 2 mo. Body weight, height, and blood pressure were measured, and BMI was calculated. Blood samples were taken from fasting subjects and serum was analyzed for total cholesterol, HDL-cholesterol, LDL-cholesterol, triacylglycerols, apolipoprotein AI, apolipoprotein B, soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and glucose. Blood pressure levels did not change throughout the study. Carbonated water intake decreased total cholesterol and LDL-cholesterol levels by 6.8% (P = 0.001) and 14.8% (P < 0.0001), respectively, whereas HDL-cholesterol concentration increased by 8.7% (P = 0.018), compared to the control period. Therefore, cardiovascular disease (CVD) risk indexes (total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol) were markedly reduced (both P < 0.0001). Soluble ICAM-1 and sVCAM-1 levels decreased by 8.4% (P = 0.007) and 14.8% (P = 0.015), respectively. Fasting serum glucose concentration decreased by 6.7% (P < 0.0001). Triacylglycerol levels did not change. Consumption of this sodium rich carbonated water can play a beneficial role in the prevention of CVD and the metabolic syndrome.
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PMID:A sodium-rich carbonated mineral water reduces cardiovascular risk in postmenopausal women. 1511 45

The metabolic syndrome and type 2 diabetes are associated with endothelial activation (and thus with inflammatory processes leading to atherosclerosis), but the mechanisms that underlie these associations are not fully understood. Endothelial intercellular adhesion molecule (ICAM)-1 plays an important role in the recruitment of immune cells during the development of atherosclerotic plaque and is a marker of inflammatory disease. We performed bivariate quantitative genetic analyses to estimate genetic and environmental correlations between circulating ICAM-1 concentration and 17 phenotypes associated with the metabolic syndrome. Our study population comprised 428 adults in 20 extended Mexican-American families from the San Antonio Family Heart Study (SAFHS). Circulating ICAM-1 concentration is heritable (h(2) = 0.56). ICAM-1 concentration showed significant positive genetic correlations (range 0.32-0.52, P < 0.05) with fasting insulin, insulin 2 h after oral glucose challenge, homeostasis model assessment of insulin resistance, BMI, waist circumference, and leptin concentration; negative genetic correlation with HDL3 cholesterol concentration; and negative environmental correlation with adiponectin concentration. Significant genetic correlations were not found between ICAM-1 and fasting or 2-h serum glucose or systolic or diastolic blood pressure. Thus, ICAM-1 expression may share common genetic modulation with traits related to obesity, insulin resistance, and HDL3 cholesterol, but not with hyperglycemia or hypertension per se.
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PMID:Intercellular adhesion molecule-1 concentration is genetically correlated with insulin resistance, obesity, and HDL concentration in Mexican Americans. 1544 2

Type 2 diabetes mellitus (DM) and the metabolic syndrome, both characterized by insulin resistance, are associated with an accelerated form of atherosclerotic vascular disease and poor outcomes following vascular interventions. These vascular effects are thought to stem from a heightened inflammatory environment and reduced bioavailability of nitric oxide (NO). To better understand this process, we characterized the vascular injury response in the obese Zucker rat by examining the expression of adhesion molecules, the recruitment of inflammatory cells, and the development of intimal hyperplasia. We also evaluated the ability of exogenous NO to inhibit the sequela of vascular injury in the metabolic syndrome. Obese and lean Zucker rats underwent carotid artery balloon injury. ICAM-1 and P-selectin expression were increased following injury in the obese animals compared with the lean rats. The obese rats also responded with increased macrophage infiltration of the vascular wall as well as increased neointima formation compared with their lean counterparts (intima/media = 0.91 vs. 0.52, P = 0.001). After adenovirus-mediated inducible NO synthase (iNOS) gene transfer, ICAM-1, P-selectin, inflammatory cell influx, and oxidized low-density lipoprotein (LDL) receptor expression were all markedly reduced versus injury alone. iNOS gene transfer also significantly inhibited proliferative activity (54% and 73%; P < 0.05) and neointima formation (53% and 67%; P < 0.05) in lean and obese animals, respectively. The vascular injury response in the face of obesity and the metabolic syndrome is associated with increased adhesion molecule expression, inflammatory cell infiltration, oxidized LDL receptor expression, and proliferation. iNOS gene transfer is able to effectively inhibit this heightened injury response and reduce neointima formation in this proinflammatory environment.
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PMID:Nitric oxide modulates vascular inflammation and intimal hyperplasia in insulin resistance and the metabolic syndrome. 1573 83

Adipose tissue has recently emerged as an active endocrine organ that secretes a variety of metabolically important substances, collectively called adipocytokines or adipokines. In this review we summarize the effects of the adipokines leptin, adiponectin, and resistin on the vasculature and their potential role for pathogenesis of vascular disease. Leptin is associated with arterial wall thickness, decreased vessel distensibility, and elevated C reactive protein (CRP) levels. Leptin possesses procoagulant and antifibrinolytic properties, and it promotes thrombus and atheroma formation, probably through the leptin receptors by promoting vascular inflammation, proliferation, and calcification, and by increasing oxidative stress. Research for development of pharmacologic antagonism for the leptin receptor is currently under way. Adiponectin inhibits the expression of the adhesion molecules ICAM-1, VCAM-1, and P selectin. Therefore, it interferes with monocyte adherence to endothelial cells and their subsequent migration to the subendothelial space, one of the initial events in the development of atherosclerosis. Adiponectin also inhibits the transformation of macrophages to foam cells in vitro and decreases their phagocytic activity. Resistin, discovered in 2001, represents the newest of the adipokines and was named for its ability to promote insulin resistance. Resistin increases the expression of the adhesion molecules VCAM-1 and ICAM-1, up-regulates the monocyte chemoattractant chemokine-1, and promotes endothelial cell activation via ET-1 release. Although many aspects of its function need further clarification, it appears that resistin will add significantly to our knowledge of the pathophysiology of vascular disease and the metabolic syndrome.
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PMID:Effects of adipocyte-derived cytokines on endothelial functions: implication of vascular disease. 1591 85

The present study was designed to examine the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation, chemotaxis, and cell adhesion. Obese men (n = 31), 15 of whom had metabolic syndrome, were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and postintervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin (for estimation of insulin sensitivity), oxidative stress-generating enzyme myeloperoxidase and marker 8-isoprostaglandin F2alpha, the inflammatory protein C-reactive protein, soluble ICAM-1 as an indicator of endothelial activation, sP-selectin as a marker of platelet activation, the chemokine macrophage inflammatory protein-1alpha, and total matrix metalloproteinase-9. Using subject sera and human aortic endothelial cell culture systems, we measured VCAM-1 cell surface abundance and monocyte chemotactic protein-1, nitric oxide, superoxide, and hydrogen peroxide production in vitro by fluorometric detection. Also determined in vitro was serum-induced, monocyte adhesion and monocyte chemotactic activity. After 3 wk, significant reductions (P < 0.05) in body mass index, all serum lipids and lipid ratios, fasting glucose, insulin, homeostasis model assessment for insulin resistance, myeloperoxidase, 8-isoprostaglandin F2alpha, C-reactive protein, soluble ICAM-1, soluble P-selectin, macrophage inflammatory protein-1alpha, and matrix metalloproteinase-9 were noted. In vitro, serum-stimulated cellular VCAM-1 expression, monocyte chemotactic protein-1 production, and fluorometric detection of superoxide and hydrogen peroxide production decreased, whereas a concomitant increase in NO production was noted (all P < 0.01). Additionally, both monocyte adhesion (P < 0.05) and MCA (P < 0.01) decreased. Nine of 15 were no longer positive for metabolic syndrome postintervention. Intensive lifestyle modification may ameliorate novel coronary artery disease risk factors in men with metabolic syndrome factors before reversal of obesity.
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PMID:Effect of a short-term diet and exercise intervention on oxidative stress, inflammation, MMP-9, and monocyte chemotactic activity in men with metabolic syndrome factors. 1661 61

Accumulating evidence has shown a strong association between the metabolic syndrome (MS) and a chronic inflammatory state predisposing to atherosclerosis. We investigated leukocyte, platelet, and endothelial activation markers and cellular interactions in 33 patients with the MS and 25 healthy controls. Using flow cytometry, we measured: (1)P-selectin expression in platelets; (2) platelet microparticles identified by CD31 expression; (3) endothelial microparticles (EMPs) identified by expression of CD31 (EMP(31)), CD62E (EMP(62E)), and CD51 (EMP(51)); (4) conjugates of leukocytes with platelet microparticles/platelets and with EMPs identified by CD54 (EMP(54)); and (5) CD11b expression in leukocytes. Patients with the MS had markedly elevated EMP(31), although EMP(62E) levels were normal, suggesting that EMP(31) levels were increased because of endothelial cell apoptosis, rather than activation. EMP(51), EMP(54)-lymphocyte conjugates, platelet expression of P-selectin, CD11b expression in leukocytes, and platelet-lymphocyte conjugates were also increased in patients with the MS. Platelet-leukocyte conjugates correlated with leukocyte activation, suggesting that platelet binding to leukocytes regulates leukocyte activation in vivo. In conclusion, our data demonstrate endothelial cell microparticle release, platelet and leukocyte activation, and increased binding of EMPs and platelets to leukocytes in patients with the MS.
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PMID:Endothelial microparticles and platelet and leukocyte activation in patients with the metabolic syndrome. 1678 24

Obesity has been linked to cardiovascular disease, hypertension, diabetes and the metabolic syndrome, with elevated markers of systemic inflammation. Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane adhesion molecule involved in leukocyte migration to sites of inflammation. In human obesity, elevated expression of the soluble form of ICAM-1 (sICAM-1) is positively correlated with abdominal fat deposition. Increases in adiposity have also been correlated with macrophage infiltration into adipose tissue. Here we investigate adipose tissue production and transcriptional regulation of ICAM-1 in a mouse model of dietary obesity. After feeding mice a high-fat diet, ICAM-1 expression in serum and adipose tissue was analyzed by ELISA, Northern blotting, real-time quantitative PCR, and flow cytometry. After 6 mo on the high-fat diet, sICAM-1 levels significantly correlated with body weight and abdominal fat mass. ICAM-1 mRNA was expressed in adipose tissue of mice, with significantly higher levels in males than females. After only 3 wk, there were adipose tissue-specific increases in mRNAs for ICAM-1, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in male mice. Analysis of the stromal-vascular fraction of male adipose tissue revealed CD11b-negative cells with increased surface ICAM-1 and CD34. We also found two populations of F4/80+, CD11b+, ICAM-1+ cells, one of which also expressed CD14 and CD11c and was increased in response to a high-fat diet. These results indicate that within 3 wk on a high-fat diet, male mice exhibited significant increases in pro-inflammatory factors and immune cell infiltration in adipose tissue that may represent links between obesity and its associated inflammatory complications.
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PMID:ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice. 1680 3

Hypertriglyceridemia is known to be associated to functional impairment of the endothelium and, consequently, to higher risk of atherosclerosis. Nevertheless, some crucial steps in the development of the atherosclerotic plaque are still unknown in primary hypertriglyceridemia. The aim of the present study was to explore the expression of soluble and leukocyte-associated cell adhesion molecules in a group of patients with primary hypertriglyceridemia, both including (n=50) and excluding (n=24) subjects with metabolic syndrome, in comparison with control normotriglyceridemic individuals (n=30). Lipid profile, CETP activity, HDL and VLDL chemical composition were evaluated. Soluble (VCAM-1, ICAM-1 and E-selectin) and leukocyte cell adhesion molecules (CD18, CD49d and CD54) were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. Patients with primary hypertriglyceridemia as compared with control subjects showed significantly higher VCAM-1 (15.6+/-4.5 ng/ml versus 13.9+/-3.8 ng/ml, respectively; p<0.05) and ICAM-1 (16.9+/-3.1 ng/ml versus 15.2+/-3.2 ng/ml, respectively; p<0.05). Regarding leukocyte cell adhesion molecules, significant increases were also detected in monocyte CD18 (398+/-180 versus 332+/-136 arbitrary units, respectively; p<0.05) and CD54 (49+/-14 versus 42+/-12 arbitrary units, respectively; p<0.05), and lymphocyte CD18 (122+/-53 versus 101+/-33 arbitrary units, respectively; p<0.05). ICAM-1 plasma levels, as well as monocyte CD18 and CD54, and lymphocyte CD18 persisted elevated even if patients with metabolic syndrome were discarded among those with hypertriglyceridemia. The increase in circulating and leukocyte cell adhesion molecules in primary hypertriglyceridemic patients would highlight the inflammatory process which is a key event in atherogenesis.
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PMID:Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia. 1753 98

Metabolic syndrome is considered a hyperinsulinemic and inflammatory state closely associated to endothelial dysfunction causing an increased incidence of ischemic cardiovascular events and high mortality. The main objective of the present study was to determine whether leukocitary and soluble cell adhesion molecules were altered in patients with metabolic syndrome in comparison with control subjects. Cell adhesion molecules, mainly of leukocitary location, have been not previously evaluated in specifically designed cross-sectional studies involving male patients with metabolic syndrome. Moreover, other circulating markers of different candidate atherogenic risk parameters were also studied and the potential existence of a progressive relation between the number of metabolic syndrome components and the above mentioned biomarkers was analyzed. Thirty one male patients with metabolic syndrome (ATPIII definition) and 56 male control subjects were studied. We evaluated different markers of insulin resistance, inflammation and atherosclerosis, as well as protective factors. Patients with metabolic syndrome showed (a) hypoadiponectinemia (4551 +/- 2302 ng/ml vs. 5865 +/- 2548 ng/ml, respectively; p<0.05), (b) an atherogenic lipid and lipoprotein profile, (c) altered HDL chemical composition accompanied by higher cholesteryl ester-triglyceride interchange carried out by CETP, (d) diminished Lp-PLA(2) activity (6.5 +/- 1.9 vs. 7.3 +/- 2.2, p<0.05, respectively), antioxidant enzyme related with LDL oxidation, which was positively associated with QUICKI and negatively with VCAM-1 and lymphocyte CD18, and (e) high soluble (VCAM-1: 17 +/-5 vs. 13 +/- 4 ng/ml, respectively; p<0.0005) and leukocyte adhesion molecule expression (monocyte CD54: 52 +/- 15 vs. 45 +/-12 arbitrary units, respectively; p<0.0005; and lymphocyte CD49d: 312 +/- 56 vs. 284 +/- 64 arbitrary units, respectively; p < 0.05). The increment in leukocyte and soluble cell adhesion molecules, crucial for leukocyte interaction with the endothelium and migration into the artery wall, in combination with the other disorders described above reinforce the presence of a clinical status with high propensity to type 2 diabetes and atherosclerotic cardiovascular disease.
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PMID:Alterations in cell adhesion molecules and other biomarkers of cardiovascular disease in patients with metabolic syndrome. 1809 67

Huang-Lian-Jie-Du-Tang (HLJDT) is a traditional Chinese herbal medicine and a potential anti-inflammatory agent. HLJDT has been used successfully to treat inflammation in diabetic rats. The current study is aimed to evaluate the effectiveness of HLJDT on myocardial remodeling in a rat model of metabolic syndrome (MS). Twenty-one MS rats were divided into two groups: the MS group and the MS+HLJDT group. Ten Wister rats were a normal control group (NC group). HLJDT (1.04 g/100g) was orally administered daily for 12 weeks in the MS+HLJDT group. The trial lasted 12 weeks. Changes of echocardiography, histological staining, transmission electron microscope (TEM), and molecular biology examinations were made. After treatment, in the MS+HLJDT group, Masson staining and echocardiography data revealed decreased collagen fibers compared with the MS group. Messenger RNA levels of IL-6, ICAM-1, TNF-alpha, TGF-beta1, NF-kappaB in left ventricular tissues were lower than in the MS group, and volume of mitochondria and the phenotype of cardiac muscle cells in TEM were close to normal. The results suggested that HLJDT reduced myocardial collagen deposition and inhibited cardiac remodeling in a rat model of MS.
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PMID:Huang-Lian-Jie-Du-Tang inhibits myocardial remodeling in a rat model of metabolic syndrome. 1869 59


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