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)

Type 2 diabetes is associated with an increased risk of nephrolithiasis, specifically in the form of uric acid (UA) nephrolithiasis. Diabetic patients who produce uric stones exhibit a low urine pH, the key factor of UA crystallization. Production of such acidic urine appears to result from the insulin-resistant state characteristic of diabetes mellitus. Insulin resistance is also involved in the pathogenesis of primary UA nephrolithiasis observed in overweight subjects with the metabolic syndrome. Therefore, UA nephrolithiasis should be considered a possible manifestation of insulin resistance, as it already is for hyperuricemia. Occurrence of UA stones in a patient, especially if overweight or hypertensive, should prompt a search for components of the metabolic syndrome in order to implement therapeutic intervention aimed at preventing the development of type 2 diabetes and atherosclerotic complications. Reciprocally, diabetologists should be aware of the risk of UA stones in their patients.
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PMID:Diabetes and nephrolithiasis. 1825 8

Although not associated with the metabolic syndrome, HCV is linked with impaired insulin signalling, insulin resistance, hypocholesterolemia and steatosis which represent a distinct HCV-associated dysmetabolic syndrome. Insulin resistance affects the development of diabetes, fibrosis, impaired response to antivirals and perhaps hepatocellular carcinoma risk. HCV infection is associated with hypocholesterolemia and steatosis reversible after sustained virologic response. A "viral", and a "metabolic" steatosis exist as function of viral genotypes. Little is known about the possible role of HCV in further components of the metabolic syndrome such as atherosclerosis, obesity, arterial hypertension, hyperuricemia and thrombotic risk factors.
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PMID:Dysmetabolic changes associated with HCV: a distinct syndrome? 1827 9

The level of serum uric acid in human has been increasing over the last decades, and correlates with an increase prevalence of renal disease and metabolic syndrome. Understanding the role of uric acid in these conditions may provide clues for preventing the current epidemic of renal disease. Controversy still remains if hyperuricemia is simply a consequence or a cause of renal disease although epidemiological studies have attempted to resolve this issue. In this review, we discuss the clinical and experimental evidence for a causal role of hyperuricemia in renal diseases and potential relationships of hyperuricemia with metabolic syndrome.
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PMID:The conundrum of hyperuricemia, metabolic syndrome, and renal disease. 1951 86

There has been an explosive increase in the prevalence of hyperuricemia and gout in Japan, suggesting the recent lifestyle change may be a key factor leading to this pathophysiological condition. In addition, people with hyperuricemia are often associated with various morbid conditions constituting the metabolic syndrome, such as abdominal obesity, hypertension, dyslipidemia and impaired glucose tolerance. Therefore, healthy lifestyle interventions would be a basic therapeutic approach not only to hyperuricemia but to metabolic syndrome, though it is not easy to promote behaviour changes. This review focuses on strategies for lifestyle intervention for clinical practice, including how we advise patients on appropriate diets, physical activity and alcoholic beverage consumption.
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PMID:[Practical strategies for lifestyle modification in people with hyperuricemia and gout treatment through diet, physical activity, and reduced alcohol consumption]. 1840 24

Metabolic syndrome is a cluster of cardiovascular risk factors such as hypertriglyceridemia, hypertension, insulin resistance, based on visceral fat accumulation. Hyperuricemia is also thought as a one of the complications of metabolic syndrome. Hyperinsulinemia caused by insulin resistance induces the low excretion type hyperuricemia. In contrast visceral fat accumulation itself causes the hypersynthetic type hyperuricemia through increased fatty acid influx into the liver. Recently hyperuricemia is suggested to play a causal role for the metabolic syndrome. Xanthine oxido-reductase, a key enzyme of uric acid metabolism was indicated as one of regulatory factors in adipocyte differentiation. These studies may shed a new light on the understanding of the relationship between hyperuricemia and metabolic syndrome.
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PMID:[Relationship between hyperuricemia and metabolic syndrome]. 1840 29

Associations between serum uric acid (UA) levels and metabolic syndrome (MetS) have been reported in cross-sectional studies. Limited information, however, is available concerning the prospective association of UA and the risk of developing MetS. The authors evaluated UA as a risk factor for incident MetS in a prospective study of 8429 men and 1260 women (aged 20-82 years) who were free of MetS and for whom measures of waist girth, resting blood pressure, fasting lipids, and glucose were taken during baseline and follow-up examinations between 1977 and 2003. Hyperuricemia was defined as >7.0 mg/dL in men and >6.0 mg/dL in women. Metabolic syndrome was defined with the National Cholesterol Education Program Adult Treatment Panel III criteria. The overall prevalence of hyperuricemia was 17%. During a mean follow-up of 5.7 years, 1120 men and 44 women developed MetS. Men with serum UA concentrations > or =6.5 mg/dL (upper third) had a 1.60-fold increase in risk of MetS (95% confidence interval, 1.34-1.91) as compared with those who had concentrations <5.5 mg/dL (lowest third). Among women, the risk of MetS was at least 2-fold higher for serum UA concentrations > or =4.6 mg/dL (P for trend = .02). Higher serum UA is a strong and independent predictor of incident MetS in men and women.
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PMID:Uric acid and the development of metabolic syndrome in women and men. 1850 69

We studied the associations between serum urate levels (determined in 503 subjects from a population of 1,344 subjects living in northern Madrid) and both the metabolic syndrome (MS) (defined by the Adult Treatment Panel III criteria) and C-reactive protein (CRP, determined in 382 subjects). MS was diagnosed in 25% (95%CI, 21-28%) and was associated with hyperuricemia (p<0.001). There was a graded increase in serum urate levels with increasing number of MS components. Urate concentrations significantly correlated with waist circumference (r=0,455, p<0.01). Serum urate was not independently associated with CRP levels. This study shows that serum urate levels are associated with the presence of MS and each of its features.
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PMID:Serum urate, metabolic syndrome, and cardiovascular risk factors. A population-based study. 1860 May 15

Hyperuricemia contributes to the pathomechanism of diseases such as renal failure, gout, tumor lysis syndrome and metabolic syndrome. Tumor lysis syndrome is a complication of malignancies caused by massive tumor cell lysis due to either spontaneous tumor cell lysis or to different therapies and it may cause hyperuricemia. Recently, for treatment of hyperuricemia the recombinant urate oxidase (rasburicase) therapy has been used. This enzyme converts uric acid with high affinity into soluble allantoin which is eliminated by the kidneys. In this reaction high concentration of hydrogen peroxide is generated. This hydrogen peroxide could cause hemolysis and especially methemoglobin formation, in case of glucose-6-phosphate-dehydrogenase and catalase deficiencies. Therefore it is recommended that these enzymes are determined before therapy. For monitoring of rasburicase therapy the determination of serum uric acid concentration is used. More than 95 per cent of Hungarian clinical laboratories are using the uricate oxidase/peroxidase reactions and hydrogen peroxide measurements in the uric acid assays. These assays may be interfered by ascorbic acid and hydrogen peroxide which is generated by rasburicase either in vivo or in vitro.
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PMID:[Rasburicase therapy may cause hydrogen peroxide shock]. 1870 12

In humans, uric acid is the main urinary metabolite of purines. Serum levels are higher compared with other mammalians. Uric acid is an antioxidant and perhaps helps to control blood pressure during a low Na+ diet through stimulation of the renin-angiotensin system. Serum uric acid is also considered a marker of tubular reabsorption and 'effective' circulating blood volume. Moreover, hyperuricemia seems to be a cofactor in Na+ -sensitive hypertension, a marker and possibly itself responsible for microvascular damage through stimulation of the renin-angiotensin system, inhibition of endothelial nitric oxide, and proliferative effects on vascular smooth muscle. As fructose-rich diets increase uric acid levels, hyperuricemia may also play a role in the metabolic syndrome, triggering insulin resistance and hypertension.A number of studies on rats rendered hyperuricemic by administration of uricase inhibitors have recently confirmed induction of arterial hypertension and microvascular injury, particularly in the remnant kidney or in cyclosporine-induced renal fibrosis.
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PMID:Uric acid: bystander or culprit in hypertension and progressive renal disease? 1885 44

Gout is the most common form of inflammatory arthritis in the elderly. In the last two decades, both hyperuricemia and gout have increased markedly and similar trends in the epidemiology of the metabolic syndrome have been observed. Recent studies provide new insights into the transporters that handle uric acid in the kidney as well as possible links between these transporters, hyperuricemia, and hypertension. The treatment of established hyperuricemia has also seen new developments. Febuxostat and PEG-uricase are two novel treatments that have been evaluated and shown to be highly effective in the management of hyperuricemia, thus enlarging the therapeutic options available to lower uric acid levels. Monosodium urate (MSU) crystals are potent inducers of inflammation. Within the joint, they trigger a local inflammatory reaction, neutrophil recruitment, and the production of pro-inflammatory cytokines as well as other inflammatory mediators. Experimentally, the uptake of MSU crystals by monocytes involves interactions with components of the innate immune system, namely Toll-like receptor (TLR)-2, TLR-4, and CD14. Intracellularly, MSU crystals activate multiple processes that lead to the formation of the NALP-3 (NACHT, LRR, and pyrin domain-containing-3) inflammasome complex that in turn processes pro-interleukin (IL)-1 to yield mature IL-1 beta, which is then secreted. The inflammatory effects of MSU are IL-1-dependent and can be blocked by IL-1 inhibitors. These advances in the understanding of hyperuricemia and gout provide new therapeutic targets for the future.
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PMID:Developments in the scientific and clinical understanding of gout. 1894 74


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