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

The Pritikin Program (Aventura, FL) involves the use of a very-low-fat, low-sodium, high-fiber diet and exercise to decrease the risk of coronary heart disease (CHD). This study evaluated the effect of short-term Pritikin therapy on the metabolic risk factors for CHD in patients with the metabolic syndrome. Sixty-seven subjects who had the metabolic syndrome and attended the Pritikin Longevity Center & Spa for 12-15 days were studied. Short-term Pritikin therapy improved most CHD risk factors: body mass index decreased by 3% (P<.001); systolic and diastolic blood pressure, and serum glucose and low-density lipoprotein cholesterol concentrations decreased by 10%-15% (P<.001); serum triglyceride concentration decreased by 36% (P<.001); and 37% of subjects no longer met National Cholesterol Education Program criteria for the metabolic syndrome. Serum high-density lipoprotein cholesterol, however, decreased by 3% (P<.05). These data demonstrate that brief treatment with a very-low-fat, low-sodium, high-fiber diet and regular exercise simultaneously improves multiple CHD risk factors in patients with the metabolic syndrome.
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PMID:Effect of short-term Pritikin diet therapy on the metabolic syndrome. 1767 87

Aldosterone concentrations are inappropriately high in many patients with hypertension, as well as in an increasing number of individuals with metabolic syndrome and sleep apnoea. A growing body of evidence suggests that aldosterone and/or activation of the MR (mineralocorticoid receptor) contributes to cardiovascular remodelling and renal injury in these conditions. In addition to causing sodium retention and increased blood pressure, MR activation induces oxidative stress, endothelial dysfunction, inflammation and subsequent fibrosis. The MR may be activated by aldosterone and cortisol or via transactivation by the AT(1) (angiotenin II type 1) receptor through a mechanism involving the EGFR (epidermal growth factor receptor) and MAPK (mitogen-activated protein kinase) pathway. In addition, aldosterone can generate rapid non-genomic effects in the heart and vasculature. MR antagonism reduces mortality in patients with CHF (congestive heart failure) and following myocardial infarction. MR antagonism improves endothelial function in patients with CHF, reduces circulating biomarkers of cardiac fibrosis in CHF or following myocardial infarction, reduces blood pressure in resistant hypertension and decreases albuminuria in hypertensive and diabetic patients. In contrast, whereas adrenalectomy improves glucose homoeostasis in hyperaldosteronism, MR antagonism may worsen glucose homoeostasis and impairs endothelial function in diabetes, suggesting a possible detrimental effect of aldosterone via non-genomic pathways.
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PMID:Aldosterone and end-organ damage. 1768 82

Lifestyle modification can reduce blood pressure and lower cardiovascular risk. Established recommendations include weight loss, sodium reduction, and increased physical activity. PREMIER studied the effects of lifestyle interventions based on established recommendations alone and with the addition of the Dietary Approaches to Stop Hypertension (DASH) dietary pattern. This analysis aimed to assess the interventions' impact on cardiometabolic variables in participants with, compared with those without, metabolic syndrome. The primary outcome was 6-month change in systolic blood pressure. Participants with prehypertension or stage-1 hypertension were randomly assigned to an advice only control group, a 6-month intensive behavioral intervention group of established recommendations (EST), or an established recommendations plus DASH group (EST+DASH). Metabolic syndrome was defined per National Cholesterol and Education Program Adult Treatment Panel III. We used general linear models to test intervention effects on change in blood pressure, lipids, and insulin resistance (homeostasis model assessment), in subgroups defined by the presence or absence of metabolic syndrome. Of 796 participants, 399 had metabolic syndrome. Both EST and EST+DASH reduced the primary outcome variable, systolic blood pressure. Within the EST+DASH group, those with and without metabolic syndrome responded similarly (P=0.231). However, within EST, those with metabolic syndrome had a poorer response, with a decrease in systolic blood pressure of 8.4 mm Hg versus 12.0 mm Hg in those without metabolic syndrome (P=0.002). Thus, metabolic syndrome attenuated the systolic blood pressure reduction of EST, but this attenuation was overcome in EST+DASH. Finally, diastolic blood pressure, lipids, and homeostasis model assessment responded similarly to both interventions regardless of metabolic syndrome status. Our data suggest that strategies for lowering BP in individuals with metabolic syndrome may be enhanced by recommendations to adopt the DASH dietary pattern.
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PMID:Effects of PREMIER lifestyle modifications on participants with and without the metabolic syndrome. 1769 24

Aldosterone is implicated in the pathogenesis of proteinuria and chronic kidney disease. We previously demonstrated the contribution of elevated serum aldosterone in the early nephropathy of SHR/NDmcr-cp (SHR/cp), a rat model of metabolic syndrome. In the present study, we investigated the effect of salt loading on renal damage in SHR/cps and explored the underlying mechanisms. SHR/cps fed a high-sodium diet for 4 weeks developed severe hypertension, massive proteinuria, and advanced renal lesions. High salt also worsened glomerular podocyte impairment. Surprisingly, selective mineralocorticoid receptor (MR) antagonist eplerenone dramatically ameliorated the salt-induced proteinuria and renal injury in SHR/cps. Although salt loading reduced circulating aldosterone, it increased nuclear MR and expression of aldosterone effector kinase Sgk1 in the kidney. Gene expressions of transforming growth factor-beta1 and plasminogen activator inhibitor-1 were also enhanced in the kidneys of salt-loaded SHR/cps, and eplerenone completely inhibited these injury markers. To clarify the discrepancy between decreased aldosterone and enhanced MR signaling by salt, we further investigated the role of oxidative stress, a putative key factor mediating salt-induced tissue damage. Interestingly, antioxidant Tempol attenuated the salt-evoked MR upregulation and Sgk1 induction and alleviated proteinuria and renal histological abnormalities, suggesting the involvement of oxidative stress in salt-induced MR activation. MR activation by salt was not attributed to increased serum corticosterone or reduced 11beta-hydroxysteroid dehydrogenase type 2 activity. In conclusion, sodium loading exacerbated proteinuria and renal injury in metabolic syndrome rats. Salt reduced circulating aldosterone but caused renal MR activation at least partially via induction of oxidative stress, and eplerenone effectively improved the nephropathy.
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PMID:Salt-induced nephropathy in obese spontaneously hypertensive rats via paradoxical activation of the mineralocorticoid receptor: role of oxidative stress. 1792 84

The metabolic syndrome (MetS) often accompanies obesity and contributes to the increased risk of atherothrombotic events with increased body fatness. Indeed, the risks for coronary artery disease and acute vascular events are greater with obesity combined with MetS compared with obesity alone. Endothelial release of tissue-type plasminogen activator (t-PA) is a key defense mechanism against thrombosis and has been shown to be impaired with obesity. The aim of the present study was to determine whether the presence of MetS exacerbates endothelial fibrinolytic dysfunction in obese adults. Net endothelial release of t-PA was determined in vivo in response to intrabrachial infusions of bradykinin and sodium nitroprusside in 47 sedentary adults: 15 normal weight (age 57 +/- 2 yr; body mass index 22.9 +/- 0.5 kg/m(2)), 14 obese but otherwise healthy (55 +/- 1 yr; 29.4 +/- 0.3 kg/m(2)), and 18 obese with MetS (55 +/- 2 yr; 32.3 +/- 1 kg/m(2)). MetS was established according to National Cholesterol Education Program ATP III criteria. Net release of t-PA antigen to bradykinin was approximately 50% lower (P < 0.01) in the obese (from 2.5 +/- 1.9 to 37.1 +/- 5.3 ng.100 ml tissue(-1).min(-1)) and obese with MetS (from 0.4 +/- 0.8 to 32.5 +/- 3.8 ng.100 ml tissue(-1).min(-1)) compared with normal-weight (from 0.9 +/- 1.0 to 74.3 +/- 8.1 ng.100 ml tissue(-1).min(-1)) subjects. However, there were no significant differences in the capacity of the endothelium to release t-PA in the obese and obese with MetS adults. These results indicate that the presence of the MetS does not worsen the obesity-related endothelial fibrinolytic dysfunction.
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PMID:Metabolic syndrome and endothelial fibrinolytic capacity in obese adults. 1795 3

This article presents results of a community-based participatory study (DASH of Soul) designed to produce soul food that meets the nutrient criteria of the DASH diet plan. DASH of Soul was tested during a 10-month period with two sub-groups of low-income African American women: (1) a focus group cooking club recruited from among "early adopters" of a previous intervention; and (2) a broader peer group dinner club recruited through a health center serving the neighborhood of the focus group. Methods for the cooking club included 10 filmed cooking labs to: (a) modify traditional soul food (MSF) to reduce food energy, total fat, saturated fat, sugar, and sodium; (b) evaluate and improve upon sensory acceptability; (c) integrate acceptable MSF into the DASH diet plan (MS-DASH); (d) produce VHS- and DVD-formatted MS-DASH cooking shows. Methods for the dinner club included monthly participation in weekly promotional dinner meetings that featured the cooking show and a different DASH food group each month for 8 months. Based on computer software analysis, the nutrient composition of a sample MS-DASH menu developed by the cooking club was consistent with nutrient levels for the DASH diet plan. The authors concluded from the focus group interviews and intercept surveys that, with continued motivation, the potential is good for the study population to make MS-DASH a lifestyle choice, reducing their risks for diet-related diseases that cluster to comprise metabolic syndrome.
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PMID:Modifying soul food for the Dietary Approaches to Stop Hypertension diet (DASH) plan: implications for metabolic syndrome (DASH of Soul). 1798 95

Cardiovascular disease has become the first cause of death in Indonesia. The highest morbidity is found in the aged, and among cardiovascular disorders or diseases, the prevalence of hypertension is the highest. Many studies of the relationship between nutritional factors and hypertension have been conducted, especially with reference to the metabolic syndrome, but studies to understand determinants of blood pressure in Indonesia are lacking. There is an urgent need to gather information about various blood pressure risk factors in Indonesian elderly, which will allow policy makers to provide appropriate intervention programs. The primary purpose of this study was to investigate various determinants of blood pressure in Indonesian elderly using multistage random sampling. Data were collected through interview using structured questionnaires, anthropometric measurements, biochemical blood analysis, and blood pressure measurements. Daily nutrient intake was analyzed using the World Food 2 Dietary Assessment Program. General Linear Model and Multiple linear regression analysis were performed to determine determinants of systolic and diastolic blood pressure. Monounsaturated fatty acid, saturated fatty acid, and sodium intake, plasma total cholesterol level, the ratio of total cholesterol to HDL-cholesterol and a sport Index were determinants of blood pressure in the normal weight elderly individuals, while potassium intake, calcium intake and BMI were determination of blood pressure in the overweight elderly individuals.
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PMID:Determinants of blood pressure among Indonesian elderly individuals who are of normal and over-weight: a cross sectional study in an urban population. 1806 39

The metabolic syndrome (MS), a cluster of risk factors, such as obesity, hyperglycemia, hypertension and dyslipidemia, contributes to the development of cardio-vascular diseases and type 2 diabetes mellitus (DM2). Insulin resistance (IR) plays a key role in MS being strongly linked to abdominal visceral fat. Treatment for obese patients with MS should aim at improving IR, delaying the onset of DM2 and at reducing cardio-vascular risk. Weight loss, first therapeutic target, may be obtained through life-style modifications and anti-obesity drugs or bariatric surgery, at need. In these patients drug therapy is necessary if therapeutic life-style changes are not sufficient. Some drugs have adverse metabolic effects, therefore the therapeutic choices must be specific and rational. Metformin, Thiazolidinediones and Acarbose are anti-hyperglycemic drugs of choice: they reduce the incidence of DM2 and IR (or improve insulin sensitivity) and they decrease or stabilize the visceral adipose tissue mass (Thiazolidinediones increases subcutaneous fat only). Also Angiotensin II receptor blockers and Angiotensin-converting enzyme inhibitors reduce the incidence of DM2 and insulin resistance and they are first-line antihypertensive drugs in MS. Calcium channel blockers, Alpha-1 antagonists and Alpha-2 agonists drugs are metabolically neutral and slight weight gains are related to the hydro-sodium retention. Beta-blockers and Diuretics, except for Indapamide and Anti-aldosterone drugs, can reduce insulin sensitivity, impair lipid profile and increase DM2 incidence; they are not first-line therapy yet they are necessary in selected cases only. Statins, Fibrates and omega-3 Fatty acids are indicated to normalize dyslipidemia. Low doses of acetylsalicylic acid are also recommended.
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PMID:[Therapeutic options for metabolic syndrome in obese patients]. 1806 54

Cardiovascular diseases continue to be the main cause of death in most industrialized countries. Endothelial dysfunction, a systemic process, is the earliest known marker of atherosclerosis and has become a major focus in acute ischemic disorders. We are investigating the hypothesis that, in these diseases, microvascular and endothelial dysfunctions occur simultaneously and precede the onset of macrovascular disease. We studied, to our knowledge for the first time in the same subjects, microvascular and endothelial functions in 11 patients with type 2 diabetes. 36 metabolic syndrome patients (NCEP-ATPIII criteria) and 25 young obese women matched with healthy controls. Micro vascular morphology and hemodynamics were evaluated non-invasively by means of nailfold videocapillaroscopy. Red blood cell velocity (RBCV, mm/s) was measured at rest and after release from 60 s of arterial occlusion (RBCVmax, mm/s) at the finger base, along with the time to reach RBCVmax (TRBCVmax, s), by video analysis with Cap Image software. Venous occlusion plethysmography was performed after intra-arterial infusions of acetylcholine and sodium nitroprusside to assess endo thelial-dependent and -independent vasodilation, respectively. We found similar results in the three groups of subjects, namely a significant decrease in RBCVmax, an increase in TRBCVmax, and a decrease in endothelial-dependent vasodilation. These findings clearly demonstrate that the two dysfunctions occur simultaneously in these groups of patients. Several mechanisms which could impair micro vascular and endothelial functions are associated with insulin resistance, and drugs that act on insulin resistance might thus be beneficial. Metformin, given to 16 first-degree relatives of patients with type 2 diabetes mellitus, who had the metabolic syndrome and normal glucose tolerance (ADA criteria), improved endothelial-dependent vasodilation and microcirculatory function. Rosiglitazone, given to 18 patients with the metabolic syndrome, enhanced vascular responses by improving endothelial function and increasing adiponectin levels. Increased triglyceride storage is often associated with insulin resistance, contributing to free fatty acid (FFA) overexposure. The two drugs tested here stimulate AMP-activated protein kinase, which promotes FFA oxidation and thus reduces oxidative stress, and might therefore attenuate endothelial lipotoxicity. The results strongly suggest that targeting micro vascular and endothelial dysfunctions in patients with metabolic disorders might help to prevent cardiovascular events, and warrant long-term clinical trials.
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PMID:[Vascular dysfunction in metabolic disorders: evaluation of some therapeutic interventions]. 1807 49

The metabolic syndrome also called syndrome X, is a constellation of interrelated risk factors of metabolic origin--metabolic risk factors--that appear to share insulin resistance as a possible pathogenetic factor that directly promote the development of atherosclerotic cardiovascular diseases and increase the risk for developing type 2 diabetes mellitus. The recommended first step for treatment of metabolic syndrome is lifestyle modifications such as weight loss, aerobic exercise, smoking cessation, and improved diet which independently improve insulin resistance and slow progression to type 2 diabetes mellitus. Even though success achieved through lifestyle modification is limited, the significance of it cannot be overemphasized. 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. Furthermore, drugs able to reduce insulin resistance, such as metformin and thiazolidinediones, already in the therapeutic armamentarium of type 2 diabetes, could be used in subjects with the metabolic syndrome as a preventive measure.
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PMID:Metabolic syndrome: are we at risk? 1809 42


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