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

Prospective trials have shown an independent negative correlation between dairy food consumption and overweight, type 2 diabetes, metabolic syndrome and ischaemic cardiovascular diseases. Large amounts of calcium can reduce intestinal fat absorption. They can also reduce lipogenesis, through an inhibitory effect on calcium calcitriol-mediated intracellular fluxes. Some soluble aminoacids appear to reduce appetite and may also improve tissular insulin sensitivity, insulin secretion, arterial pressure and cardiovascular morbidity. Milk and dairy foods are recommended for patients with obesity, diabetes, hypertension and metabolic syndrome, and also for patients at risk. The high quality and low price of dairy proteins must be underlined. Controversy surrounding the possible atherogenic effect of dairy fatty acids means that fat-free milk and other dairy foods without added sugar should be preferred. Contraindications include lactose maltolerance and milk protein allergy.
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PMID:[Milk and dairy products in the prevention and therapy of obesity, type 2 diabetes and metabolic syndrome]. 1902 47

Over the past 10 years, major progress has been made in the pathogenesis of uric acid and calcium stones. These advances have led to our further understanding of a pathogenetic link between uric acid nephrolithiasis and the metabolic syndrome, the role of Oxalobacter formigenes in calcium oxalate stone formation, oxalate transport in Slc26a6-null mice, the potential pathogenetic role of Randall's plaque as a precursor for calcium oxalate nephrolithiasis, and the role of renal tubular crystal retention. With these advances, we may target the development of novel drugs including (1) insulin sensitizers; (2) probiotic therapy with O. formigenes, recombinant enzymes, or engineered bacteria; (3) treatments that involve the upregulation of intestinal luminal oxalate secretion by increasing anion transporter activity (Slc26a6), luminally active nonabsorbed agents, or oxalate binders; and (4) drugs that prevent the formation of Randall's plaque and/or renal tubular crystal adhesions.
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PMID:Recent advances in the pathophysiology of nephrolithiasis. 1964 81

The current obesity epidemic in the United States has deleterious effects on the health of the population. Temporally related to the increase in obesity is an increase in the prevalence of urolithiasis. Epidemiologic studies have shown that the incident stone risk increases with body mass index. Obesity can increase stone risk in multiple ways. Excess nutritional intake increases traffic of lithogenic substances such as calcium, oxalate, and uric acid. Metabolic syndrome, commonly associated with obesity, alters renal acid-base metabolism, resulting in a lower urine pH and increased risk of uric acid stone disease. The low urine pH is caused by deficient ammonia production, which appears to be related to insulin resistance. Even weight-loss programs to combat obesity can influence stone risk. Contemporary bariatric surgery has been shown to frequently cause hyperoxaluria with associated stone formation and even oxalate nephropathy. Commonly used low-carbohydrate diets increase the risk of both calcium and uric acid stones. Certainly, the many health risks of obesity, including urolithiasis, necessitate weight loss, but recognition of the potential complications of such therapies is required to prevent induction of new and equally severe medical problems. The optimal approach to weight control that minimizes stone risk needs to be determined.
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PMID:Obesity and urolithiasis. 1909 1

This study was performed to evaluate the relationship between serum phosphate levels and cardiovascular risk factors and metabolic syndrome components in a cross-sectional survey. Plasma phosphate was measured by immunoturbidimetry in 46,798 subjects over 20 years of age with an estimated GFR>or=60 mL/(min 1.73 m(2)) who participated in a health-check survey at the Kangbuk Samsung Hospital in South Korea. The median plasma phosphate level was 3.49+/-0.44 mg/dL and the mean estimated GFR was 77.46+/-8.51 mL/(min 1.73 m(2)). We found that serum phosphate levels had a positive correlation with total cholesterol, HDL-C, lipoprotein a, apolipoprotein A1, calcium, and albumin. In addition, serum phosphate levels had a negative correlation with age, body mass index, uric acid, fasting glucose, insulin, HOMA-IR, HS-CRP, triglyceride levels, systolic blood pressure, diastolic blood pressure, and waist circumference (P<0.001). In conclusion, we found that a high phosphate level is correlated with cardiovascular disease while a lower phosphate level is correlated with metabolic syndrome. Serum phosphate levels that were too high or too low correlated with cardiovascular risk factors and elements of metabolic syndrome, respectively, showing that it may be important to maintain an appropriate level of phosphate for the prevention of cardiovascular events and metabolic syndrome.
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PMID:Serum phosphate levels and the risk of cardiovascular disease and metabolic syndrome: a double-edged sword. 1910 Oct 54

Certain cardiovascular drugs have adverse effects on glucose homeostasis, which may lead to important long-term implications for increased risks of adverse outcomes. Thiazide diuretics, niacin, and beta-adrenergic blockers impair glucose homeostasis. However, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated beneficial metabolic effects. The newer vasodilating beta-blocking agents and calcium antagonists appear to be metabolically neutral. These considerations, in addition to meticulous attention to blood pressure control and lifestyle changes, have the potential to beneficially modify glycemia and long-term risks. These considerations have particular importance in younger patients who may also have pre-diabetes or the metabolic syndrome and who are likely to require therapy over the course of decades.
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PMID:Cardiovascular therapies and associated glucose homeostasis: implications across the dysglycemia continuum. 1917 14

Deficiency of minerals causes functional abnormality of enzymes, frequently resulting in metabolic disturbance. We investigated possible relationship between minerals and metabolic syndrome by analysis of hair tissue minerals. We selected 848 subjects older than 20 years of age at Ajou University Hospital from May 2004 to February 2007. We excluded the subjects who had cancers, steroid and thyroid medication, and incomplete record from the study. Finally, 343 subjects were eligible. We performed cross-sectional analysis for the relationship between minerals and metabolic syndrome. The contents of calcium, magnesium, and copper in the metabolic syndrome group were significantly lower than those of the normal group, whereas the amounts of sodium, potassium, and mercury in the metabolic syndrome group were significantly higher than those of the normal group. By dividing the subjects into quartile with the level of calcium, magnesium, and mercury concentrations, we carried out logistic regression analysis to study the subjects and found that the subjects in the third quartile of calcium and magnesium concentrations had significantly lower odds ratio (OR) of the metabolic syndrome compared with that of the lowest quartile group [OR = 0.30, confidence interval (CI) = 0.10-0.89; OR = 0.189, CI = 0.063-0.566] and that the subjects in the highest mercury quartile had significantly higher OR of the metabolic syndrome compared with that of the lowest mercury quartile group (OR = 7.35, CI = 1.73-31.1). As part of the metabolic syndrome, the optimal calcium and magnesium concentrations in hair tissue may reflect decreased risk of metabolic syndrome, whereas high mercury concentration in hair tissue may indicate increased risk of metabolic syndrome.
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PMID:Hair tissue mineral analysis and metabolic syndrome. 1922 98

This study is to evaluate beta cell function and investigate the mechanism of impaired pancreatic islet beta cell function in monosodium glutamate (MSG) obese rat with insulin resistance, an animal model of metabolic syndrome. Insulin tolerance test was used to screen MSG obese rats with insulin resistance. Blood concentrations of glucose, triglyceride, total cholesterol and insulin were determined. Beta cell function was assessed with hyperglycemic clamp technique. The morphological alterations in pancreas and changes of islet beta cell mass were evaluated by hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining. Lipid, oxidative stress relevant factors, nitric oxide (NO) level and activity of ATPase in pancreas and pancreatic mitochondrial were tested. The MSG obese rats with insulin resistance could be validated as a typical metabolic syndrome animal model possessing increased fasting plasma triglycerides and insulin (P < 0. 001), markedly decreased weight indices of pancreas and impaired glucose-stimulated insulin secretion. Hematoxylin-eosin (HE) and Gomori aldehyde fuchsin staining showed increased adipocytes and fibroplasia deposition in pancreas and reduced beta cell mass. The increased contents of triglyceride and NO level, the decreased SOD levels and activities of total ATPase (P < 0.001), Na+-K+-ATPase (P < 0.001) and Ca2+-Mg2+-ATPase (P < 0.01) were observed in pancreas and its mitochondria versus normal rat. The study demonstrates that accumulation of lipids in pancreas could lead to increased systemic indicators of inflammation, such as NO, which may influence the activities of several kinds of ATPase in cell membranes and interfere the ion transport, substance metabolism and energy production in pancreas. Finally the MSG obese rats characterized with metabolic syndrome displayed an impairment of beta cell function.
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PMID:[A preliminary study on the mechanism of impaired beta cell function in monosodium glutamate obese rat with insulin resistance]. 1923 28

The authors compared the metabolic syndrome status and Framingham 10-year coronary heart disease risk score (FRS) with the coronary artery calcification (CAC) in subclinical atherosclerosis. In all, 356 consecutive patients who underwent coronary artery calcium scanning were studied. Participants' metabolic syndrome status (by National Cholesterol Education Program Adult Treatment Panel III [NCEP ATP III] guidelines) and FRS were measured. The association between the metabolic syndrome, diabetes mellitus (DM), FRS, and CAC was analyzed by multivariable logistic regression analyses. These analyses were adjusted for demographics, age, sex, and conventional cardiovascular risk factors. The prevalence of significant CAC (CAC score >/=100) in those with DM, the metabolic syndrome, and neither condition was 64%, 43%, and 24%, respectively. The receiver operating characteristic C statistic for the prediction of significant CAC by the NCEP ATP III criteria for FRS, the metabolic syndrome, and DM was 0.61, 0.67, and 0.72, respectively, and increased significantly to 0.78 and 0.90 respectively for the metabolic syndrome and DM when added to the prediction models (P<.0001). This study suggests that the metabolic syndrome and DM are associated with increased risk of subclinical atherosclerosis. In addition, the presence of the metabolic syndrome or DM with increased FRS has incremental value over the FRS, DM, or the metabolic syndrome alone in predicting significant CAC.
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PMID:Measures of coronary artery calcification and association with the metabolic syndrome and diabetes. 1924 10

The metabolic syndrome is a clustering of risk factors known to promote or increase the risk of diabetes development and subsequent cardiovascular disease. Screening for subclinical atherosclerosis using new imaging technologies or novel biomarkers could help to further risk-stratify patients with metabolic syndrome. In particular, noninvasive imaging of carotid intima-media thickness and coronary artery calcium scoring seem to have promising prognostic value in identifying patients at high risk. Early identification could lead to improved patient or physician adherence to risk-reducing behaviors or interventions and improve clinical outcomes.
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PMID:Metabolic syndrome, cardiovascular risk and screening for subclinical atherosclerosis. 1929 65

A benefit-risk evaluation of the evidence for including dairy foods in the diet is presented. For many persons dairy products provide a substantial portion of essential nutrients, but especially calcium, potassium, and magnesium. Dietary supplements and fortified foods can be alternative sources of these nutrients, although other components of dairy foods such as amino acid composition and conjugated linoleic acid may be instrumental in the benefits associated with dairy product consumption for bone health and reduced risk of stroke, metabolic syndrome, and some cancers. Newer evidence shows that protein-induced calciuria does not have a detrimental effect on net calcium retention, and the concentrations of hormones in milk are not outside of the range of endogenous concentrations. Increased dietary protein, including from milk, can elevate serum concentrations of insulin-like growth factor I, which has an unknown relation to cancer. The concern over consumption of milk leading to increased risk of prostate cancer through reduction of serum 1,25-dihydroxyvitamin D, a potent anti-prostate cancer hormone, has been resolved with new evidence that local production of this hormone is independent of diet. Overall, evidence suggests that being a lactovegetarian has greater health benefits and reduced health risks than being a vegan.
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PMID:Should dairy be recommended as part of a healthy vegetarian diet? Point. 1932 71


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