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

LDL receptor (LDLR)-null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome, have vascular calcification (VC) worsened by chronic kidney disease (CKD) and ameliorated by bone morphogenetic protein-7 (BMP-7), an efficacious agent in treating animal models of renal osteodystrophy. Here, LDLR-/- high-fat-fed mice without CKD were shown to have significant reductions in bone formation rates, associated with increased VC and hyperphosphatemia. Superimposing CKD resulted in a low turnover osteodystrophy, whereas VC worsened and hyperphosphatemia persisted. BMP-7 treatment corrected the hyperphosphatemia, corrected the osteodystrophy, and prevented VC, compatible with skeletal phosphate deposition leading to reduced plasma phosphate and removal of a major stimulus to VC. A pathologic link between abnormal bone mineralization and VC through the serum phosphorus was supported by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in this model of the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to low bone turnover rates, producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through deposition of phosphate and increased bone formation.
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PMID:Low turnover osteodystrophy and vascular calcification are amenable to skeletal anabolism in an animal model of chronic kidney disease and the metabolic syndrome. 1574 94

We have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreases the serum phosphate. Most recently, these observations were rediscovered in low-density lipoprotein receptor null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance). We had demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial type. We have shown that VC is worsened by CKD and ameliorated by bone morphogenetic protein -7 (BMP-7). The finding that high-fat-fed low-density lipoprotein receptor null animals without CKD have hyperphosphatemia led us to examine the skeletons of these mice. We found significant reductions in bone formation rates, associated with increased VC and superimposing CKD results in the adynamic bone disorder (ABD), while VC was worsened and hyperphosphatemia persisted. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. BMP-7 treatment corrected the ABD and corrected hyperphosphatemia, compatible with BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. Thus, in the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to ABD producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through increased bone formation and skeletal deposition of phosphate, and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury before demonstrable hyperphosphatemia, and they are preventable and treatable. Therefore, early intervention in CKD is warranted and may affect mortality of the disease.
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PMID:Connections between vascular calcification and progression of chronic kidney disease: therapeutic alternatives. 1633 68

In two independent and separate studies, we have shown that renal injury and chronic kidney disease (CKD) directly inhibit skeletal anabolism, and that stimulation of bone formation decreased the serum phosphate. In the first study, the serum Ca PO(4), parathyroid hormone (PTH), and calcitriol were maintained normal after renal ablation in mice, and even mild renal injury equivalent to stage 3 CKD decreased bone formation rates. More recently, these observations were rediscovered in low-density lipoprotein receptor null (LDLR-/-) mice fed high-fat/cholesterol diets, a model of the metabolic syndrome (hypertension, obesity, dyslipidemia and insulin resistance). We demonstrated that these mice have vascular calcification (VC) of both the intimal atherosclerotic type and medial calcification. We have also shown that VC is made worse by CKD and ameliorated by bone morphogenetic protein-7 (BMP-7). The finding that high-fat fed LDLR-/- animals with CKD had hyperphosphatemia which was prevented in BMP-7-treated animals lead us to examine the skeletons of these mice. It was found that significant reductions in bone formation rates were associated with high-fat feeding, and superimposing CKD resulted in the adynamic bone disorder (ABD), while VC was made worse. The effect of CKD to decrease skeletal anabolism (decreased bone formation rates and reduced number of bone modelling units) occurred despite secondary hyperparathyroidism. The BMP-7 treatment corrected the ABD and hyperphosphatemia, owing to BMP-7-driven stimulation of skeletal phosphate deposition reducing plasma phosphate and thereby removing a major stimulus to VC. A pathological link between abnormal bone mineralization and VC through the serum phosphorus was demonstrated by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in the metabolic syndrome with CKD, a reduction in bone forming potential of osteogenic cells leads to the ABD producing hyperphosphatemia and VC, processes ameliorated by BMP-7, in part through increased bone formation and skeletal deposition of phosphate and in part through direct actions on vascular smooth muscle cells. We have demonstrated that the processes leading to vascular calcification begin with even mild levels of renal injury affecting the skeleton before demonstrable hyperphosphatemia and that they are preventable and treatable. Therefore, early intervention in the skeletal disorder associated with CKD is warranted and may affect mortality of the disease.
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PMID:Function and effect of bone morphogenetic protein-7 in kidney bone and the bone-vascular links in chronic kidney disease. 1688 97

A model of chronic kidney disease (CKD)-induced vascular calcification (VC) that complicates the metabolic syndrome was produced. In this model, the metabolic syndrome is characterized by severe atherosclerotic plaque formation, hypertension, type 2 diabetes, obesity, and hypercholesterolemia, and CKD stimulates calcification of the neointima and tunica media of the aorta. The CKD in this model is associated the adynamic bone disorder form of renal osteodystrophy. The VC of the model is associated with hyperphosphatemia, and control of the serum phosphorus both in this animal model and in humans has been preventive in the development of VC. This article reports studies that demonstrate reduction of established VC by the addition of sevelamer carbonate to the diets of this murine metabolic syndrome model with CKD. Sevelamer, besides normalizing the serum phosphorus, surprisingly, reversed the CKD-induced trabecular osteopenia. Sevelamer therapy increased osteoblast surfaces in the metaphyseal trabeculae of the tibia and femur. It also increased osteoid surfaces and, importantly, bone formation rates. In addition, sevelamer was found to be effective in decreasing serum cholesterol levels. These results suggest that sevelamer may have important actions in decreasing diabetic and uremic vasculopathy and that sevelamer carbonate may be capable of increasing bone formation rates that are suppressed by diabetic nephropathy.
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PMID:Reversal of the adynamic bone disorder and decreased vascular calcification in chronic kidney disease by sevelamer carbonate therapy. 1718 86

Although there are no official recommendations for specific nutrient intakes in premature infants after hospital discharge, it is agreed that the goal should be to achieve the body composition and rate of growth of that of a normal fetus of the same postmenstrual age during the entire first year of life. A general recommendation to use the special formulas designed for preterm infants after hospital discharge in place of the formulas for term infants cannot be made from the available evidence at this time. Infants fed human milk after discharge are of the greatest concern as human milk does not in theory meet the requirements for growth in these infants. Such infants should remain on supplemental vitamins and Fe while breastfeeding, and growth as well as serum levels of phosphorus and alkaline phosphatase should be carefully monitored. The increased risk of preterm infants for obesity and the metabolic syndrome secondary to the metabolic/nutritional events early in life (programming) is likely to be small compared with the contribution of other risk factors, such as parental size, weight as an adolescent, and various lifestyle factors such as physical activity.
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PMID:Post-discharge nutrition: what does the evidence support? 1746 93

A number of cross-sectional analysis studies have been conducted to determine the relationships between serum uric acid and related variables or clinical manifestations. However, few data related to changes in serum uric acid within the same cohort population at two separate periods of time have been reported. In this study, we investigated the changes in serum uric acid in a population from baseline to 1-year follow-up and examined the associations with related parameters and medical conditions. A total of 1,437 eligible male subjects who underwent 2 medical examinations at a health promotion center at an interval of approximately 12 months were enrolled in this study. Data were obtained from routine physical assessments such as blood pressure, height, waist circumference, blood analyses for liver function, renal function, lipid profile, and electrolytes, along with standardized questionnaires including self-reported data. In this population, serum uric acid was significantly increased at 1-year follow-up compared with the baseline level (5.94 +/- 1.20 vs 5.99 +/- 1.22, p = 0.003). Changes of some confounders such as total bilirubin, creatinine, BUN, phosphorus, total cholesterol, and triglyceride were significantly associated with changes in serum uric acid. Among them, serum creatinine may be the most influential in determining the serum uric acid level (odds ratio = 21.691, 95%CI = 5.110-92.086). A change of serum uric acid over 1 year did not seem to affect changes in the clinical status for some medical conditions including hypertension, diabetes mellitus, cardiovascular disease, and metabolic syndrome. This analysis showed that a change in serum creatinine level between baseline and 1-year follow-up might be the most potent factor affecting a change in serum uric acid in healthy, male subjects. Changes of serum uric acid did not show any meaningful impact on the development of hypertension, heart failure, diabetes mellitus, and metabolic syndrome in this 1-year follow-up study.
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PMID:Change in serum uric acid between baseline and 1-year follow-up and its associated factors in male subjects. 1787 70

Obesity and the related metabolic syndrome have become a worldwide epidemic. Inactivity appears to be a primary causative factor in the pathogenesis of this obesity and metabolic syndrome. There are two possible, perhaps not mutually exclusive, events that may lead to intramyocellular lipid accumulation and mitochondrial dysfunction in patients with obesity. First, obesity, with high intake-associated lipid accumulation in muscle may interfere with cellular mitochondrial function through generation of reactive oxygen species leading to lipid membrane peroxidative injury and disruption of mitochondrial membrane-dependent enzymes. This in turn leads to impaired oxidative metabolism. Secondly, a primary defect in mitochondrial oxidative metabolism may be responsible for a reduction in fatty acid oxidation leading to intramyocellular lipid accumulation as a secondary event. Non-invasive techniques such as proton (1H) and phosphorus (31P) magnetic resonance spectroscopy, coupled with specific magnetic resonance imaging techniques, may facilitate the investigation of the effects of various ergometric interventions on the pathophysiology of obesity and the metabolic syndrome. Exercise has positive effects on glucose metabolism, aerobic metabolism, mitochondrial density, and respiratory chain proteins in patients with metabolic syndrome, and we propose that this may be due to the exercise effects on AMP kinase, and a prospective physiological mechanism for this benefit is presented. A physiological model of the effect of intramyocellular lipid accumulation on oxidative metabolism and insulin mediated glucose uptake is proposed.
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PMID:Skeletal muscle metabolic dysfunction in obesity and metabolic syndrome. 1838 Feb 75

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

The U.S. Dietary Guidelines for Americans recommends 3 cups of low fat milk or equivalent daily for most calorie levels [1]. Milk provides over 10% of the requirement for calcium, vitamin D, magnesium, phosphorus, potassium, riboflavin, protein, and carbohydrates for most people. Obtaining adequate intakes of calcium, potassium, and magnesium without milk in the diet requires effort. Milk has bioactive ingredients that may play unique roles in health. Benefits of dairy consumption are associated with reduced risk of low bone mass, stroke, metabolic syndrome, and some cancers. Concerns over milk consumption have focused on saturated fats historically. More research is needed to resolve potential concerns of milk consumption and risk of several disorders including ovarian cancer and soft tissue calcification.
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PMID:Role of dairy beverages in the diet. 2013 73

Although metabolic syndrome (MS) is associated with low bone mineral density (BMD) in the general population, it is unknown whether similar associations exist in patients with chronic kidney disease. We investigated risk factors that can lead to low BMD values in hemodialysis patients with MS according to the diagnostic criteria set by International Diabetes Federation (IDF) in this study. A total of 64 patients with MS undergoing hemodialysis and 60 hemodialysis patients who were matched in terms of age, gender, and hemodialysis duration without MS were enrolled in the study. BMD was measured at lumbar vertebra (LV) and femur neck (FN) by performing dual-energy X-ray absorptiometry (DEXA). LV and/or FN-BMD results revealed that, of the hemodialysis patients with MS, 45% had osteoporosis and 48% had osteopenia. On the other hand, of the hemodialysis patients without MS, 42% had osteoporosis and 52% had osteopenia. Low BMD values were observed to be correlated negatively with age, hemodialysis period, and parathormone (PTH) both in the group with MS and in the group without MS. Height, weight, BMI, calcium, phosphorus, alkaline phosphatase, heparin, and vitamin D therapy and urea reduction ratio were not established to be correlated with BMD.
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PMID:Risk factors leading to reduced bone mineral density in hemodialysis patients with metabolic syndrome. 2044 86


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