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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

We recently established that the Dahl salt-sensitive rat, a model for genetic salt-sensitive hypertension, was insulin resistant. This study was undertaken to evaluate whether other features of the metabolic syndrome developed in this animal model. Two groups of 16 Dahl salt-sensitive (DSS) rats and their controls, Dahl salt-resistant (DSR) rats were used. For eight weeks, half of each group was fed a standard diet with low sodium content (85 mmol Na/kg diet) while the remainder was fed a high-sodium diet (340 mmol Na/kg diet). Weekly systolic and diastolic blood pressures were measured for all animals. At the end of eight weeks, the urinary Na(+)/K(+) ratio, fasting blood glucose, plasma uric acid and blood lipids were determined for all animals. The same parameters were measured in two additional matched weanling DSS and DSR groups of eight animals each. Adult DSS rats became hypertensive, with the DSS high-salt group exhibiting both genetic hypertension and the pressor effects of a high-salt diet. The DSS high-salt and weanling groups exhibited a lowered urinary Na(+)/K(+) ratio, indicative of greater sodium retention, when compared to their respective DSR groups (p < 0.05). No strain differences were observed in the uric acid levels. However a high-salt diet in both DSS and DSR groups elevated uric acid levels. Weanling and DSS high-salt groups showed increased total plasma cholesterol when compared to their corresponding DSR groups (p < 0.05). In addition, the DSS high-salt group also had both increased total plasma cholesterol and high-density lipoprotein (HDL) cholesterol when compared to the DSS low-salt group (p < 0.05). No significant differences in blood glucose and plasma insulin were observed in the adult groups. The weanling DSS group showed a marked hyperinsulinaemia, suggesting that DSS rats were possibly insulin resistant even before hypertension was fully established. This could indicate that insulin resistance and hypertension may be inherited as separate traits that develop in a parallel but independent manner.
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PMID:Facets of the metabolic syndrome in Dahl hypertensive rats. 1514 36

The metabolic syndrome, in which insulin resistance is the core feature, is associated both with dysregulation of thrombosis/fibrinolysis and erythrocyte sodium/lithium countertransport (SLC). To investigate this further we designed a cross-sectional study to examine whether factors involved in coagulation- and fibrinolysis systems were associated with SLC independently of insulin resistance in 93 58-year-old men. SLC was in univariate analysis positively correlated with PAI-1 activity (r = 0.35, p <0.01), tPA antigen (r = 0.38, p <0.01), von Willebrand factor (r = 0.25, p <0.05), protein S (r = 0.26, p <0.05), and C (r = 0.30, p <0.01), and negatively associated with tPA activity(r = -0.28, p <0.01). Since these correlations could be influenced by the components of the metabolic syndrome itself, a separate analysis with adjustment for glucose infusion rate (GIR), plasma insulin, body fat, sagittal diameter of the abdomen (SD) and log serum triglyceride concentration (TG) was conducted. Then SLC was associated with tPA antigen independent of GIR, plasma insulin, body fat, SD and TG. SLC was also associated with protein C independent of GIR, insulin, body fat and SD but not TG. In conclusion, we found a relationship between SLC and the fibrinolytic system that was not related to the metabolic syndrome.
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PMID:Erythrocyte sodium/lithium countertransport is associated with thrombotic and fibrinolytic factors in 58-year-old men. 1517 2

Patients with the metabolic syndrome have three or more of five cardiovascular risk factors and increased oxidative stress, arterial stiffness and pressor responses to exercise, which may contribute to their threefold greater risk for coronary heart disease. In addition to lowering basal blood pressure (BP), angiotensin receptor blockers (ARBs) may benefit metabolic syndrome patients by reducing oxidative stress, arterial stiffness, and pressor responses to exercise. Twelve patients, 7 women and 5 men, with the metabolic syndrome (aged 45 +/- 2 years, BP 145 +/- 5/85 +/- 2 mm Hg, waist girth 110 +/- 3 cm, triglycerides 186 +/- 23 mg/dL, HDL cholesterol 44 +/- 2 mg/dL, glucose 99 +/- 3 mg/dL) were studied off medications, while on modest sodium restriction ( approximately 100 mmol/d). Patients were randomized to the ARB losartan or placebo for 3 weeks then crossed over to the complement for 3 weeks. Studies were performed at the end of each phase following an overnight fast. Serum lipids and biomarkers of oxidative stress (F2-isoprostanes, thiobarbituric acid reacting substances) were unchanged by losartan, whereas large artery elasticity at rest, measured with the HDI PulseWave, increased from 13.6 +/- 0.7 on placebo to 16.2 +/- 1.1 mL/mm Hg on losartan, P <.05. Losartan lowered systolic BP pre-exercise from 142 +/- 3 to 131 +/- 3 mm Hg (P <.001) and systolic BP after 6 min of treadmill exercise from 192 +/- 6 to 169 +/- 5 mm Hg (P <.001). Losartan lowered systolic BP (-23 +/- 3 v -11 +/- 2 mm Hg, P <.05) and pulse pressure (-4 +/- 1 v -15 +/- 2 mm Hg, P <.05) more during exercise than rest. Losartan reduces the pressor response to exercise, perhaps by enhancing arterial compliance. In addition to lowering basal BP, angiotensin receptor blockade in patients with metabolic syndrome improves arterial compliance and reduces pressor reactivity to exercise.
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PMID:Angiotensin receptor blockade improves arterial distensibility and reduces exercise-induced pressor responses in obese hypertensive patients with the metabolic syndrome. 1517 18

Hypertension is one of most important components of metabolic syndrome. Main etiology of metabolic syndrome is supposed to be due to insulin resistance. Insulin resistance/hyperinsulinemia induces blood pressure elevation by sodium retention, activation of sympathetic nervous system and renin-angiotensin system(RAS) and promotion of vascular cell growth. Moreover, activated RAS, actually angiotensin II, and salt intake lead insulin resistance by inhibiting insulin signaling. Our laboratory revealed the close relationship between the vascular RAS and the action of insulin on the vasculature. This section reviewed recent understandings about hypertension in metabolic syndrome focusing on its pathophysiologic mechanisms and antihypertensive therapy.
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PMID:[Hypertension]. 1520 48

The constellation of dyslipidemia (hypertriglyceridemia and low levels of high-density lipoprotein cholesterol), elevated blood pressure, impaired glucose tolerance, and central obesity is identified now as metabolic syndrome, also called syndrome X. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the U.S. population. The National Cholesterol Education Program-Adult Treatment Panel III has identified metabolic syndrome as an indication for vigorous lifestyle intervention. Effective interventions include diet, exercise, and judicious use of pharmacologic agents to address specific risk factors. Weight loss significantly improves all aspects of metabolic syndrome. Increasing physical activity and decreasing caloric intake by reducing portion sizes will improve metabolic syndrome abnormalities, even in the absence of weight loss. Specific dietary changes that are appropriate for addressing different aspects of the syndrome include reducing saturated fat intake to lower insulin resistance, reducing sodium intake to lower blood pressure, and reducing high-glycemic-index carbohydrate intake to lower triglyceride levels. A diet that includes more fruits, vegetables, whole grains, monounsaturated fats, and low-fat dairy products will benefit most patients with metabolic syndrome. Family physicians can be more effective in helping patients to change their lifestyle behaviors by assessing each patient for the presence of specific risk factors, clearly communicating these risk factors to patients, identifying appropriate interventions to address specific risks, and assisting patients in identifying barriers to behavior change.
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PMID:Metabolic syndrome: time for action. 1522 52

This study tested the hypothesis that evolution of the metabolic syndrome in obese Zucker rats (OZR) leads to impaired dilator reactivity of cerebral resistance arteries vs. responses determined in lean Zucker rats (LZR). Middle cerebral arteries (MCA) from 17-wk-old male LZR and OZR were isolated and cannulated with glass micropipettes. Vascular reactivity was assessed in response to challenge with ACh, sodium nitroprusside (SNP), reductions and elevations in Po2, 5-HT, and increased intralumenal pressure. Vessels were treated with the free radical scavenger 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol) to assess the role of superoxide production in altering reactivity, and passive vascular wall mechanics was assessed in each vessel. Vascular superoxide production was assessed in isolated arteries using fluorescence microscopy. Vessel dilation to ACh and hypoxia was impaired in OZR vs. LZR, although responses to SNP were normal. Vessel constriction to 5-HT, elevated Po2, and elevated intralumenal pressure was enhanced in OZR vs. LZR. Fluorescence microscopy demonstrated an increased superoxide production in arteries of OZR vs. LZR, correctable by incubation with tempol. Although treatment of vessels from OZR with tempol improved dilation to ACh and hypoxia, constrictor responses to 5-HT, elevated Po2, and pressure were not altered by tempol treatment. Indexes of vessel wall mechanics were comparable between groups. These results suggest that vasodilator reactivity of MCA of OZR in response to endothelium-dependent dilator stimuli is impaired vs. LZR and that this may represent a reduced bioavailability of signaling molecules due to oxidant scavenging. However, oxidative stress-independent increases in myogenic tone and constrictor reactivity may contribute to blunted dilator responses of cerebral microvessels.
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PMID:Oxidant stress and constrictor reactivity impair cerebral artery dilation in obese Zucker rats. 1551 4

1. Abnormal vasorelaxation responses are seen in the context of various disease states, including obesity, hypertension, hyperlipidemia and diabetes. Metabolic syndrome, which is characterized by the concomitant presence of all of these disease states, develops spontaneously in the SHR/NDmcr-cp (cp/cp) rat (SHR-cp). The goal of the present study was to determine whether abnormal vasorelaxation responses were present with metabolic syndrome. 2. Acetylcholine-induced endothelial-dependent relaxation was significantly enhanced in aortas isolated from SHR-cp at the age of 18 weeks when compared to that from control rats [lean littermates SHR/NDmcr-cp (+/+) (SHR)]. In contrast, endothelium-independent relaxation in response to sodium nitroprusside was equally attenuated in the two rat groups compared with normotensive Wistar-Kyoto rats. 3. These results suggest that endothelial nitric oxide (NO) production increased in the aorta of SHR-cp as compared to SHR. This may compensate for the concomitant impairment in the NO-mediated relaxation response in smooth muscle cells, that probably results from hypertension. Enhanced NO production may result from a variety of factors, including increases in oxidative stress in the context of the metabolic syndrome.
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PMID:Characteristics of vasorelaxation responses in a rat model of metabolic syndrome. 1564 91

Hypertension is related to sodium intake, and many patients with essential hypertension are overweight and have the metabolic syndrome. We therefore studied microsatellite markers close to the thiazide-sensitive Na-Cl cotransporter on chromosome 16 and a quantitative trait locus for abdominal obesity-metabolic syndrome (AOMS2) on chromosome 17, which have been found to be linked to hypertension in a previous genome scan in Chinese. There were 84 hypertensive subjects (44 men, 40 women, age 53+/-13 years) and 88 normotensive controls (40 men, 48 women, age 54+/-13 years) recruited. Specific oligonucleotide primers were used to amplify genomic DNA spanning the microsatellite markers D16S3396 and D17S1303 that consist of ATA and GATA repeats, respectively. We did not find any association between D16S3396 and blood pressure. In contrast, the distribution of D17S1303 genotypes differed between hypertensive subjects and normal controls (P = 0.014). The number of GATA repeats correlated inversely with diastolic blood pressure (r = -0.18, P = 0.02) and body mass index (r = -0.12, P = 0.01). Nine GATA repeats in D17S1303 were associated with hypertension (OR 2.19, 95% CI 1.08-4.44, P = 0.027), while 14 GATA repeats were associated with normotension (OR 0.26, 95% CI 0.10-0.66, P = 0.002). The diastolic blood pressure in those with or without the (GATA)9 allele was 85.9+/-13.6 and 79.2+/-13.6 mmHg respectively (P = 0.01), and in those with or without the (GATA)14 allele it was 73.8+/-11.0 and 81.8+/-14.0 mmHg respectively (P = 0.003). Our results provide further evidence that a gene predisposing to hypertension in Chinese is in the vicinity of the microsatellite D17S1303.
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PMID:Association of essential hypertension with a microsatellite marker on chromosome 17. 1571 82

Lipids play varied and critical roles in metabolism, with function dramatically modulated by the individual fatty acid moities in complex lipid entities. In particular, the fatty acid composition of membrane lipids greatly influences membrane function. Here we consider the role of dietary fatty acid profile on membrane composition and, in turn, its impact on prevalent disease clusters of the metabolic syndrome and mental illness. Applying the classical physiological conformer-regulator paradigm to quantify the influence of dietary fats on membrane lipid composition (i.e. where the membrane variable is plotted against the same variable in the environment--in this case dietary fats), membrane lipid composition appears as a predominantly regulated parameter. Membranes remain relatively constant in their saturated (SFA) and monounsaturated (MUFA) fatty acid levels over a wide range of dietary variation for these fatty acids. Membrane composition was found to be more responsive to n-6 and n-3 polyunsaturated fatty acid (PUFA) levels in the diet and most sensitive to n-3 PUFA and to the n-3/n-6 ratio. These differential responses are probably due to the fact that both n-6 and n-3 PUFA classes cannot be synthesised de novo by higher animals. Diet-induced modifications in membrane lipid composition are associated with changes in the rates of membrane-linked cellular processes that are major contributors to energy metabolism. For example, in the intrinsic activity of fundamental processes such as the Na+/K+ pump and proton pump-leak cycle. Equally, dietary lipid profile impacts substantially on diseases of the metabolic syndrome with evidence accruing for changes in metabolic rate and neuropeptide regulation (thus influencing both sides of the energy balance equation), in second messenger generation and in gene expression influencing a range of glucose and lipid handling pathways. Finally, there is a growing literature relating changes in dietary fatty acid profile to many aspects of mental health. The understanding of dietary lipid profile and its influence on membrane function in relation to metabolic dysregulation has exciting potential for the prevention and treatment of a range of prevalent disease states.
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PMID:Dietary fats and membrane function: implications for metabolism and disease. 1572 42


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