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)

Serum total calcium concentrations (CaT) were increased, ionized calcium concentrations (CaI) normal, and the CaI/CaT ratios decreased in 125 geriatric diabetics as compared with 379 non-diabetic controls. In the whole population of 558 consecutive geriatric inpatients, the CaI/CaT ratios were inversely correlated with body weight, diastolic blood pressure and plasma glucose. The findings and calculations help to explain some inconsistencies and discrepancies in previous studies concerning calcaemia in diabetes, hypertension and the 'metabolic syndrome' of clustered risk factors for cardiovascular diseases. They also demonstrate that CaT and the 'correction' of CaT for serum albumin concentration can be biased in diabetes and other conditions closely associated with cardiovascular risks. Increased serum free fatty acids could at least in part explain low ratios.
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PMID:Low serum ionized to total calcium ratio: association with geriatric diabetes mellitus and with other cardiovascular risk factors? 227 24

We investigated the association between fasting insulin concentration--an indicator of insulin resistance in nondiabetic individuals--cardiovascular risk factors, and coronary heart disease in a study of 390 men in the town of Zutphen. In 1990, an extensive examination was carried out on the participating men (aged 70 to 89 years). Fasting insulin levels were determined and a number of other risk factors measured. Known and newly diagnosed diabetics were excluded from the data analyses. Fasting insulin concentration was significantly associated with levels of glucose, triglycerides, uric acid, serum albumin, creatinine, and fibrinogen as well as resting heart rate. Inverse associations with high-density lipoprotein cholesterol and factor VII activity were observed. These results were independent of confounding factors such as age, body mass index, ratio of subscapular to triceps skinfold thicknesses, cigarette smoking, physical activity, and alcohol consumption. Men with a fasting insulin level higher than 80 pmol/L (highest quartile of the distribution) had a significantly higher prevalence of coronary heart disease and especially of myocardial infarction. This result was independent of potential confounding variables as well as of possible intermediates (total and high-density lipoprotein cholesterol, hypertension, serum triglycerides, fasting glucose, and other risk factors related to fasting insulin) (odds ratio, 2.2; 95% confidence interval, 1.2-4.0). No association between fasting insulin level and hypertension or blood pressure was observed. These results show that fasting insulin is an important indicator of coronary heart disease in elderly men. Clotting factors, resting heart rate, uric acid, serum albumin, and creatinine may also play a role in this metabolic syndrome.
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PMID:Hyperinsulinemia, risk factors, and coronary heart disease. The Zutphen Elderly Study. 791 15

The pathological significance of advanced glycation end product (AGE)-modified proteins deposited in several lesions is generally accounted for by their cellular interaction via the AGE receptors and subsequent acceleration of the inflammatory process. In this study, we focused on two AGE receptors-specifically, the role of SR-A in pathogenesis of diabetic nephropathy and the role of CD36 in AGE-induced downregulation of leptin by adipocytes. In terms of SR-A, diabetic wild-type mice exhibited increased urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion, whereas SR-A-knockout mice showed reduced glomerular size and mesangial matrix area. In these diabetic SR-A-knockout mice, the number of macrophages that infiltrated into glomeruli was remarkably reduced (P < 0.05), suggesting that SR-A-dependent glomerular migration of macrophages plays an important role in the pathogenesis of diabetic nephropathy. In terms of CD36, incubation of glycolaldehyde-modified bovine serum albumin (GA-BSA) with 3T3-L1 adipocytes reduced leptin secretion by these cells. The binding of GA-BSA to these cells and subsequent endocytic degradation were effectively inhibited by a neutralizing anti-CD36 antibody. AGE-induced downregulation of leptin was protected by N-acetyl-cysteine, an antioxidant. These results indicate that the interaction of AGE ligands with 3T3-L1 adipocytes via CD36 induces oxidative stress and leads to inhibition of leptin expression by these cells, suggesting a potential link of this phenomenon to exacerbation of the insulin sensitivity in metabolic syndrome.
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PMID:Pathological roles of advanced glycation end product receptors SR-A and CD36. 1603 91

Previous observations by us have clarified that proteins modified by advanced glycation end products (AGEs) are recognized as effective ligands by CD36-overexpressed CHO cells and undergo receptor-mediated endocytosis. CD36, a member of the class B scavenger receptor family, also acts as a fatty acid transporter in adipocytes. Oxidized low-density lipoprotein (Ox-LDL), a ligand for CD36, is known to upregulate CD36 by activating peroxisome proliferator-activated receptor gamma (PPAR-gamma) in macrophages, whereas PPAR-gamma ligands such as troglitazone and 15-deoxy-delta12,14-prostaglandin J2 decrease leptin secretion from adipocytes. The purpose of this study was to examine effects of AGE ligands on leptin expression in adipocytes. Glycolaldehyde-modified bovine serum albumin (GA-BSA) decreased leptin expression at both the protein and mRNA levels in 3T3-L1 adipocytes and mouse epididymal adipocytes. The binding to and subsequent endocytic degradation of GA-BSA by 3T3-L1 adipocytes were effectively inhibited by a neutralizing anti-CD36 antibody. These results indicate that the ligand interaction of GA-BSA with CD36 leads to downregulation of leptin expression in 3T3-L1 adipocytes, suggesting that AGE-induced leptin downregulation is linked to reduction of the insulin sensitivity in metabolic syndrome.
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PMID:Glycolaldehyde-modified bovine serum albumin downregulates leptin expression in mouse adipocytes via a CD36-mediated pathway. 1603 95

Serum albumin is a maker of nutritional status and possesses antioxidative properties. Here, we have sought to investigate the mode of association between serum albumin levels, metabolic syndrome, and carotid atherosclerosis by analyzing the data of the cross-sectional data from 8143 individuals who underwent general health screening test. After adjusting for age, total cholesterol, and smoking status, the highest quartile of serum albumin (>or=4.7 g/dL) was associated with increased prevalence of metabolic syndrome with an odds ratio of 1.80 (95% CI 1.41-2.23, P<0.0001) in women, and 1.60 (95% CI 1.44-1.78, P<0.0001) in men, when compared to the lowest serum albumin quartile (<4.3g/dL). By contrast, when compared with the lowest quartile, the highest quartile of serum albumin was associated with reduced prevalence of carotid plaque with an odds ratio of 0.62 (95% CI 0.42-0.91, P<0.001) in women, and 0.76 (95% CI 0.62-0.93, P<0.01) in men, and for carotid intima-media thickening with an odds ratio of 0.57 (95% CI 0.35-0.94, P<0.05) in women, and 0.71 (95% CI 0.55-0.92, P<0.01) in men. Our data showed that higher serum albumin was inversely associated with the prevalence of early carotid atherosclerosis, although it was positively associated with the prevalence of metabolic syndrome. Whether these observations are in part explained by the antioxidative properties of albumin requires further investigation.
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PMID:Association between serum albumin, carotid atherosclerosis, and metabolic syndrome in Japanese individuals. 1690 16

Generalized capillary dysfunction is a morbid element in the metabolic syndrome, and it is likely involved in its complications. We tested the hypothesis that vast amounts of serum albumin previously observed in kidneys of rats with the metabolic syndrome were caused, in part, by leakage from renal peritubular capillaries. We report herein large scale leaks of plasma fluid in peritubular capillaries of rats with the metabolic syndrome. This finding was directly demonstrated in vivo, and the presence of leftover albumin residue confirmed the leak in postmortem kidney specimens. Moreover, renal interstitial fibrosis and tubular atrophy were found in a distribution similar to the leaked renal albumin in obese rats. We suggest that there is an important link between peritubular capillary damage and interstitial fibrosis, represented as tubulointerstitial disease in the metabolic syndrome. We propose that maintenance of the peritubular microcirculation may improve renal outcomes in diabetes and the metabolic syndrome.
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PMID:Microcirculation: nexus of comorbidities in diabetes. 1749 88

Many proteins have been identified as targets for S-nitrosylation, including structural and signaling proteins, a nd ion channels. S-nitrosylation plays an important role in regulating their activity and function. We used human serum albumin (HS A), a major endogenous NO traffic protein, and studied the effect of mediators on S-nitrosylation processes which control NO bioactivity. By using NOC-7, S-nitrosoglutathione, and activated RAW264.7 cells as NO-donors we found that high-affinity binding of endogenous ligands (Cu(2+), bilirubin and fatty acid) can affect these processes. It is likely that the same effects take place in many clinical situations characterized by increased fatty acid concentrations in plasma such as type II diabetes and the metabolic syndrome. Thus, endogenous ligands, changing their plasma concentrations, could be a novel type of mediator of S-nitrosylation not only in the case of HSA but also for other target proteins.
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PMID:Effects of endogenous ligands on the biological role of human serum albumin in S-nitrosylation. 1827 39

The effects of nonglycated bovine serum albumin (BSA) and advanced glycosylation end products of BSA (AGE-BSA) on vascular responses of control and metabolic syndrome (MS) rats characterized by hypertriglyceridemia, hypertension, hyperinsulinemia, and insulin resistance were studied. Albumin and in vitro prepared AGE-BSA have vascular effects; however, recent studies indicate that some effects of in vitro prepared AGEs are due to the conditions in which they were generated. We produced AGEs by incubating glucose with BSA for 60 days under sterile conditions in darkness and at 37 degrees C. To develop MS rats, male Wistar animals were given 30% sucrose in drinking water since weanling. Six month old animals were used. Blood pressure, insulin, triglycerides, and serum albumin were increased in MS rats. Contraction of aortic rings elicited with norepinephrine was stronger. There were no effects of nonglycated BSA or AGE-BSA on contractions in control or MS rats; however, both groups responded to L-NAME, an inhibitor of nitric oxide synthesis. Arterial relaxation induced using acetylcholine was smaller in MS rats. Nonglycated BSA and AGE-BSA significantly diminished relaxation in a 35% in the control group but the decrease was similar when using nonglycated BSA and AGE-BSA. This decrease was not present in the MS rats and was not due to increased RAGEs or altered biochemical characteristics of BSA. In conclusion, both BSA and AGE-BSA inhibit vascular relaxation in control artic rings. In MS rats the effect is lost possibly due to alterations in endothelial cells that are a consequence of the illness.
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PMID:Glycation does not modify bovine serum albumin (BSA)-induced reduction of rat aortic relaxation: the response to glycated and nonglycated BSA is lost in metabolic syndrome. 1845 31

We investigated the effect of body composition, nutrition, inflammation and iron status on insulin resistance in patients with long-term hemodialysis. We selected 43 stable end-stage chronic renal failure patients, on maintenance hemodialysis. We evaluated the nutritional status, body composition by subjective global assessment (SGA), anthropometric measurements (BMI and waist circumference), bioelectrical impedance analysis and biochemical parameters measurements [serum albumin, cholesterol, HDL-cholesterol, triglyceride, hematocrit, hemoglobin, iron, ferritin, calcium, phosphorus, intact parathormone (i-PTH), TNF-alpha, IL-6 and high sensitivity C-reactive protein]. All parameters were evaluated by comparisons between HOMA-IR tertiles, and after simple regression analysis, by backward multivariate regression analysis we identified independent variables for IR. As the tertile of HOMA-IR increased, serum level of glucose, insulin, and waist increascd, whereas HDL-cholesterol level decreased, or the prevalence of the metabolic syndrome increased across the tertiles of HOMA-IR. After adjustment for gender, age, hemodialysis duration, ferritin, phosphorus, waist and total fat percentages, multivariate regression analysis was performed and the association with HOMA-IR was still strong only for serum levels of iron and TNF-alpha. That explains 16% of the total variation in HOMA-IR. Our results suggest that the increase of IR in end-stage chronic renal failure patients on hemodialysis could be related to anemia and particularly to iron overload. Moreover, chronic inflammatory status with over-production of adipokine TNF-alpha participate in the pathogenesis of IR too. The present study demonstrated that adipokine TNF-alpha and serum iron participated as independent predictors in the pathogenesis of insulin resistance on long-term hemodialysis patients.
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PMID:The effect of nutritional status, body composition, inflammation and serum iron on the developement of insulin resistance among patients on long-term hemodialysis. 1892 54

Abnormalities in nutritional status of peritoneal dialysis (PD) patients include too high body mass (overweight, obesity), too low body mass (underweight, starvation) or changes in body composition (malnutrition) without or with normal body weight. In vivo neutron activation analysis is considered the reference gold standard for the determination of protein malnourishment in end-stage renal disease patients, but body mass index (BMI) is the most frequently used parameter in nutritional assessment surveys. The association between BMI and outcome of PD patients is controversial, but so-called obesity paradox (the higher BMI the longer survival) remains frequently reported. The use of metabolic syndrome with high BMI as a crucial component is not more predictable in the prognosis of outcome in PD patients than using separately each risk factor of metabolic syndrome. Underweight/starvation is univocally underlined as associated with morbidity and mortality, but prevalence of severe undernutrition is decreasing over last decades, at least in well developed countries. PD patients may also present features of malnutrition without decreased body mass or even with increased body weight. It mainly concerns to deficiencies of vitamins, minerals and trace elements. Serum albumin concentration has serious limitations as a marker of nutritional status, because is influenced by volemic status and inflammation. Nutritional interventions in undernourished patients (oral, intestinal or intravenous feeding, amino acid peritoneal solution, supplementation of vitamins and trace elements) may correct deficiencies, but their influence on PD patients survival remains unclear.
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PMID:The role of nutritional status in the outcome of peritoneal dialysis patients. 1985 51


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