UMLS:C0948265 - FACTA Search

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

Recently the definition, the pathophysiology and even the clinical utility of metabolic syndrome (MS) have been discussed. The risk induced by each component of the metabolic syndrome is higher than the risk induced by MS alone. MS alone is, in fact, a weaker predictor of cardiovascular disease than diabetes. New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. IGF/IGFBP system could be a link between insulin resistance and cardiovascular disease. RBP-4 can attenuate insulin signalling in skeletal muscle and induce hepatic gluconeogenesis. The belief that insulin-resistance is the main cause of MS could change in favour of the adipose tissue dysfunction. The most common cause of a reduced capacity of the adipose tissue to store fats is the increased dietary intake, also present in lipodistrophy, type 1 diabetes mellitus and polycystic ovarian syndrome. The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. The comprehension of adipose tissue dysfunction mechanisms offers new possibilities of prevention and therapy.
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PMID:[Metabolic syndrome: from insulin resistance to adipose tissue dysfunction]. 1849 27

Some studies have reported a possible relationship between endothelial nitric oxide synthase (eNOS) and metabolic syndrome (MS), which is associated with an increased risk for cardiovascular disease. A recent meta-analysis study found the eNOS G894T polymorphism to be associated with ischemic heart disease. Here, we examine the association of eNOS G894T polymorphism with MS in a Chinese population (n = 397). The eNOS T+ (TT and GT) genotypes (56.92% vs 38.86%; odds ratio, 2.08; 95% confidence interval, 1.21-3.56; P = .007) and T allele (33.08% vs 23.34%; odds ratio, 1.62; 95% confidence interval, 1.08-2.44; P = .019) were significantly more frequent in subjects who had MS. Furthermore, subjects with eNOS T+ genotypes had significantly higher plasma C-reactive protein levels as compared with GG subjects (P = .004). This study shows that, in a Chinese population, eNOS G894T polymorphism is associated with an elevated C-reactive protein level and MS.
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PMID:The association of endothelial nitric oxide synthase G894T polymorphism with C-reactive protein level and metabolic syndrome in a Chinese study group. 1864 Mar 91

The number one cause of mortality in the US is cardiovascular related disease. Future predictions do not see a reduction in this rate especially with the continued rise in obesity [P. Poirier, et al., Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss, Arterioscler Thromb Vasc Biol. 26(5), (2006) 968-976.; K. Obunai, S. Jani, G.D. Dangas, Cardiovascular morbidity and mortality of the metabolic syndrome, Med.Clin. North Am., 91(6), (2007) 1169-1184]. Even so, potential molecular therapeutic targets for cardiac gene delivery are in no short supply thanks to continuing advances in molecular cardiology. However, efficient and safe delivery remains a bottleneck in clinical gene therapy [O.J. Muller, H.A. Katus, R. Bekeredjian, Targeting the heart with gene therapy-optimized gene delivery methods, Cardiovasc Res, 73(3), (2007) 453-462]. Viral vectors are looked upon favorably for their high transduction efficiency, although their ability to elicit toxic immune responses remains [C.F. McTiernan, et al., Myocarditis following adeno-associated viral gene expression of human soluble TNF receptor (TNFRII-Fc) in baboon hearts, Gene Ther, 14(23), (2007) 1613-1622]. However, this high transduction does not necessarily translate into improved efficacy [X. Hao, et al., Myocardial angiogenesis after plasmid or adenoviral VEGF-A(165) gene transfer in rat myocardial infarction model, Cardiovasc Res., 73(3), (2007) 481-487]. Naked DNA remains the preferred method of DNA delivery to cardiac myocardium and has been explored extensively in clinical trials. The results from these trials have demonstrated efficacy in regard to secondary end-points of reduced symptomatology and perfusion, but have failed to establish significant angiogenesis or an increase in myocardial function [P.B. Shah, D.W. Losordo, Non-viral vectors for gene therapy: clinical trials in cardiovascular disease, Adv Genet, 54, (2005) 339-361]. This may be due in part to reduced transfection efficiency but can also be attributed to use of suboptimal candidate genes. Currently, polymeric non-viral gene delivery to cardiac myocardium remains underrepresented. In the past decade several advances in non-viral vector development has demonstrated increased transfection efficiency [O.J. Muller, H.A. Katus, R. Bekeredjian, Targeting the heart with gene therapy-optimized gene delivery methods, Cardiovasc Res, 73(3), (2007) 453-462]. Of these polymers, those that employ lipid modifications to improve transfection or target cardiovascular tissues have proven themselves to be extremely beneficial. Water-soluble lipopolymer (WSLP) consists of a low molecular weight branched PEI (1800) and cholesterol. The cholesterol moiety adds extra condensation by forming stable micellular complexes and was later employed for myocardial gene therapy to exploit the high expression of lipoprotein lipase found within cardiac tissue. Use of WSLP to deliver hypoxia-responsive driven expression of hVEGF to ischemic rabbit myocardium has proven to provide for even better expression in cardiovascular cells than Terplex and has demonstrated a significant reduction in infarct size (13+/-4%, p<0.001) over constitutive VEGF expression (32+/-7%, p=0.007) and sham-injected controls (48+/-7%). A significant reduction in apoptotic values and an increase in capillary growth were also seen in surrounding tissue. Recently, investigations have begun using bioreducible polymers made of poly(amido polyethylenimines) (SS-PAEI). SS-PAEIs breakdown within the cytoplasm through inherent redox mechanisms and provide for high transfection efficiencies (upwards to 60% in cardiovascular cell types) with little to no demonstrable toxicity. In vivo transfections in normoxic and hypoxic rabbit myocardium have proven to exceed those results of WSLP transfections by 2-5 fold [L.V. Christensen, et al., Reducible poly(amido ethylenediamine) for hypoxia-inducible VEGF delivery, J Control Release, 118(2), (2007) 254-261]. This new breed of polymer(s) may allow for decreased doses and use of new molecular mechanisms not previously available due to low transfection efficiencies. Little development has been seen in the use of new gene agents for treatment of myocardial ischemia and infarction. Current treatment consists of using mitogenic factors, described decades earlier, alone or in combination to spur angiogenesis or modulating intracellular Ca2+ homeostasis through SERCA2a but to date, failed to demonstrate clinical efficacy. Recent data suggests that axonal guidance cues also act on vasculature neo-genesis and provide a new means of investigation for treatment.
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PMID:Novel polymer carriers and gene constructs for treatment of myocardial ischemia and infarction. 1866 30

Hearts of NaCl-induced hypertensive-glucose intolerant (HGI) rats develop reduced infarcts after ischemia-reperfusion injury (IRI) than their hypertensive (H) counterparts. Because high intake of saturated fat is a major risk factor for ischemic heart disease, we tested the hypothesis that chronic (18 weeks) consumption of a high saturated fat diet increases susceptibility to IRI, an effect more marked in the HGI rats than in the H rats. The fat-fed H (HFAT) rat displayed significantly higher body weight and plasma leptin content compared to the H, HGI, or fat-fed HGI (HGIFAT) rats which all showed similar values. In contrast, plasma triglyceride concentration was significantly higher in the HGIFAT rat than in the other three groups. Plasma insulin concentration was similar in the two H groups but higher than that of the two HGI groups. Compared to the H rat, the HGI rat was markedly glucose intolerant, with fat feeding causing comparable worsening of glucose intolerance in each group. The HGIFAT rats displayed a reduction in baseline myocardial contractility and relaxation and a higher end-diastolic pressure compared to the other three groups. Infarct size was significantly lower in the HGI rats than in the H rats. Although fat feeding did not affect infarct size of the H rat, it worsened that of the HGIFAT rat thereby abrogating the differential that existed between the H and HGI rats. In conclusion, excess fat feeding impairs myocardial function of HGI rats and increases their susceptibility to IRI. These findings are of relevance to the metabolic syndrome that manifests as a cluster of insulin resistance, dyslipidemia, and systemic hypertension.
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PMID:Myocardial ischemic-reperfusion injury in a rat model of metabolic syndrome. 1871 42

In recent years, the association between hyperlipidemia and the development of arteriosclerosis has been addressed in several studies. Rabbit models of hypertriglyceridemia (TGH) and postprandial hypertriglyceridemia (PHT) have been developed at the authors' institute. TGH rabbits manifest pathology similar to that of humans with TGH, such as xanthoma, in addition to atherosclerosis of arterioles. Furthermore, PHT rabbits show visceral obesity, insulin resistance, and impaired glucose tolerance, with pathologic features similar to those of the metabolic syndrome assumed to be the cause of human ischemic heart disease. This study was designed to investigate the histopathologic features of TGH and PHT rabbits. TGH rabbits showed advanced aortic atherosclerosis, accompanied by intimal thickening of coronary and renal arteries, fatty liver changes, and xanthoma. PHT rabbits demonstrated aortic intimal thickening and hepatic fatty degeneration. The results of this study suggest that TGH and PHT rabbits are useful animal models for studying human hyperlipidemia and metabolic syndrome and the cardiovascular diseases that result from these conditions.
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PMID:Pathologic findings in rabbit models of hereditary hypertriglyceridemia and hereditary postprandial hypertriglyceridemia. 1900 73

Limited information is available regarding risk of cardiovascular disease and trends for the metabolic syndrome in Asia. We examined the impact of the metabolic syndrome and its components on risk of cardiovascular disease among middle-aged Japanese according to four criteria. We followed 2,613 subjects from a rural Japanese community who participated in cardiovascular health examinations between 1990 and 1993. After 27,477 person-years of follow-up through 2003, there were 42 incidents of ischemic heart disease, 73 total strokes (54 ischemic and 18 hemorrhagic), and 115 total cases of cardiovascular disease. The metabolic syndrome was defined according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATPIII), American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI), International Diabetes Federation (IDF), and Japanese criteria. The multivariable hazard ratios (95%CI) associated with the metabolic syndrome based on NCEP-ATPIII criteria were 2.1 (1.1-4.0) for ischemic heart disease, 1.7 (1.0-2.7) for total stroke, 2.0 (1.2-3.5) for ischemic stroke, 1.1 (0.4-2.8) for hemorrhagic stroke, 2.0 (1.3-3.1) for ischemic cardiovascular disease, and 1.7 (1.2-2.5) for total cardiovascular disease. The population-attributable fractions of the metabolic syndrome based on NCEP-ATPIII criteria were 26-27% for ischemic heart disease and ischemic stroke and 20% for total cardiovascular disease. The metabolic syndrome based on AHA/NHLBI, IDF and Japanese criteria had weaker associations with risk of cardiovascular disease, and the association with risk of ischemic heart disease was not statistically significant. The metabolic syndrome based on NCEP-ATP III criteria predicted risks of ischemic heart disease, ischemic stroke and total cardiovascular disease, whereas that based on three other criteria predicted them less effectively.
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PMID:Metabolic Syndrome and the Risk of Ischemic Heart Disease and Stroke among Middle-Aged Japanese. 1913 99

Diabetes, one of the major risk factors of metabolic syndrome culminates in the development of Ischemic Heart Disease (IHD). Refined diets that lack micronutrients, mainly trivalent chromium (Cr(3+)) have been identified as the contributor in the rising incidence of diabetes. We investigated the effect of niacin-bound chromium (NBC) during ischemia/reperfusion (IR) injury in streptozotocin induced diabetic rats. Rats were randomized into: Control (Con); Diabetic (Dia) and Diabetic rats fed with NBC (Dia+NBC). After 30 days of treatment, the isolated hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. NBC treatment demonstrated significant increase in left ventricular functions and significant reduction in infarct size and cardiomyocyte apoptosis in Dia+NBC compared with Dia. Increased Glut-4 translocation to the lipid raft fractions was also observed in Dia+NBC compared to Dia. Reduced Cav-1 and increased Cav-3 expression along with phosphorylation of Akt, eNOS and AMPK might have resulted in increased Glut-4 translocation in Dia+NBC. Our results indicate that the cardioprotective effect of NBC is mediated by increased activation of AMPK, Akt and eNOS resulting in increased translocation of Glut-4 to the caveolar raft fractions thereby alleviating the effects of IR injury in the diabetic myocardium.
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PMID:Niacin bound chromium treatment induces myocardial Glut-4 translocation and caveolar interaction via Akt, AMPK and eNOS phosphorylation in streptozotocin induced diabetic rats after ischemia-reperfusion injury. 1902 47

In this study, we aimed to examine the impact of the metabolic syndrome and its components on the risk of cardiovascular disease among a relatively less-obese population. A total of 8249 men and 15 064 women, aged 40-69 years, with no history of ischemic heart disease, stroke and/or cancer completed a risk-factor survey between 1993 and 1995. The metabolic syndrome was defined based on modified criteria of the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) and the International Diabetes Federation (IDF). Systematic cardiovascular surveillance was carried out throughout 2003, and 693 events of ischemic heart disease and stroke were identified. We observed significant associations of the metabolic syndrome with the risk of ischemic heart disease and ischemic stroke, but not with hemorrhagic stroke. The multivariable hazard ratio (95% confidence interval) of ischemic heart disease among men for the metabolic syndrome based on the AHA/NHLBI criteria was 2.25 (1.44-3.51) and that of ischemic stroke was 1.88 (1.40-2.52). The respective hazard ratios for the metabolic syndrome based on the IDF criteria were 1.61 (0.99-2.64) for ischemic heart disease and 1.94 (1.41-2.68) for ischemic stroke. The population-attributable fraction (PAF) of the metabolic syndrome based on the AHA/NHLBI criteria was higher than that based on the IDF criteria: 19 vs. 12% (P for difference=0.003) for ischemic cardiovascular disease among men, because non-overweight men with >or=2 risk factors were also at high risk (20% of the PAF). Our data suggest that the metabolic syndrome based on the AHA/NHLBI criteria predicts ischemic cardiovascular disease better than the syndrome based on the IDF criteria, because of the exclusion of non-overweight high-risk individuals from the reference group.
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PMID:The impact of the metabolic syndrome and its components on the incidence of ischemic heart disease and stroke: the Japan public health center-based study. 1926 90

The blood pressure lowering effect of a fruit and vegetable-rich diet is a necessary dietary lifestyle measure now included the guidelines for the management of arterial hypertension. Furthermore, flavonoids represent a major class of plant polyphenolics. The present review addresses the antihypertensive effect of quercetin, one of the most abundant flavonoids present in fruits and vegetables, and probably the best studied flavonoid because of its high biological activity. Quercetin has been shown to induce a progressive, dose-dependent and sustained reduction in blood pressure when given chronically in several rat models of hypertension, including spontaneously hypertensive rats, L-NAME-treated rats, DOCA-salt hypertensive rats, two-kidney one-clip Goldblatt rats, rats with aortic constriction and Dahl salt-sensitive hypertensive rats. Quercetin was also effective in reducing blood pressure in rat models of metabolic syndrome, including the obese Zucker rats as well as rats treated with a high-sucrose, high-fat diet. Quercetin also prevented morphological and functional changes in the heart, vessels and kidney, while increasing production of reactive oxygen species associated with hypertension. A high dose of quercetin also reduced blood pressure in stage 1 hypertensive patients in a randomized, double-blind, placebo-controlled, crossover study. Since raised blood pressure is the major cause of stroke as well as an important risk factor for ischemic heart disease, we propose that the blood pressure-lowering effect of quercetin could be an important mechanism contributing to the reduced risk of myocardial infarction and stroke observed with fruit and vegetables-rich diets, and possibly with flavonoid-rich diets.
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PMID:Antihypertensive effects of the flavonoid quercetin. 1930 94

We examined the association between bone mineral density (BMD) and cardiovascular risk in a group of premenopausal women selected from the Southern province of Sri Lanka. One hundred six previously healthy premenopausal volunteers (aged 30-54 yr) were recruited by open invitations. Subjects with previous history of diabetes, hypertension, epilepsy, chronic renal or liver disease, hyperlipidemia, ischemic heart disease, endocrine diseases, or prolonged inflammatory conditions were excluded. Subjects who were taking medications that can affect bone density, blood sugar, serum lipids, or blood pressure (BP) were also excluded. Women with the history of previous fractures were not excluded. BMDs in the spine, hip, and total body (TB) were measured using a Hologic Discovery scanner (Hologic Inc, Bedford, MA). BP, fasting glucose, and fasting lipids were also measured. Independent of body mass index (BMI) and age, TB bone mineral content (BMC) and spine BMD showed inverse and significant correlations with total cholesterol (TC), low density cholesterol, and the ratio between TC and high density lipoprotein cholesterol (r ranged from -0.24 to -0.27, p<0.05 for all). The highest mean lipid levels were seen among the women in the lowest third of spine BMD, whereas women in the upper third of spine BMD had the lowest lipid levels. The number of women with metabolic syndrome in the 3 tirtiles of spine BMD was not significantly different. Fasting glucose or BP had no association with either BMD or BMC. In conclusion, our data demonstrates an association, independent of age and BMI, between BMD and BMC or lipid levels among previously healthy, premenopausal women. This may explain the high cardiovascular risk seen in women with osteoporosis in old age.
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PMID:Osteoporosis and cardiovascular risk among premenopausal women in Sri Lanka. 1932 32

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