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)

Emerging evidence suggests that increased dietary consumption of fructose in Western society may be a potentially important factor in the growing rates of obesity and the metabolic syndrome. This review will discuss fructose-induced perturbations in cell signaling and inflammatory cascades in insulin-sensitive tissues. In particular, the roles of cellular signaling molecules including nuclear factor kappa B (NFkB), tumor necrosis factor alpha (TNF-alpha), c-Jun amino terminal kinase 1 (JNK-1), protein tyrosine phosphatase 1B (PTP-1B), phosphatase and tensin homolog deleted on chromosome ten (PTEN), liver X receptor (LXR), farnesoid X receptor (FXR), and sterol regulatory element-binding protein-1c (SREBP-1c) will be addressed. Considering the prevalence and seriousness of the metabolic syndrome, further research on the underlying molecular mechanisms and preventative and curative strategies is warranted.
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PMID:Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms. 1760 9

The aim of the present study was to investigate the relationships between metabolic syndrome and atherosclerosis in 57 Japanese type 2 diabetic patients. Metabolic syndrome was diagnosed based on the criteria raised by the Japan Internal Medicine Society. Insulin resistance was estimated by the insulin resistance index of homeostasis model assessment. Ultrasonographically measured carotid atherosclerosis, brachial-ankle pulse wave velocity (ba-PWV), and ankle brachial index (ABI) were used to assess the degree of atherosclerosis. Of 57 patients, 25 were diagnosed as having metabolic syndrome. The patients with metabolic syndrome had significantly higher levels of waist circumference, insulin, insulin resistance index of homeostasis model assessment, systolic and diastolic blood pressures, and serum triglycerides, and lower concentrations of adiponectin. However, there was no significant difference in age, sex, glycosylated hemoglobin (hemoglobin A1c), fasting glucose, leptin, and tumor necrosis factor system activities including tumor necrosis factor alpha between the 2 groups. Furthermore, no significant difference was observed in the degree of carotid atherosclerosis (intimal-medial thickness in plaque-free segments: 0.72+/-0.03 vs 0.72+/-0.02 mm, P=.435; carotid stenosis in plaque segments: 6.6%+/-3.0% vs 6.6%+/-1.7%, P=.497), ba-PWV (1676+/-56 vs 1654+/-44, P=.380), and ABI (1.16+/-0.01 vs 1.15+/-0.01, P=.245) between the 2 groups. From these results, it can be suggested that metabolic syndrome, an insulin-resistant state, is not associated with carotid atherosclerosis, ba-PWV, or ABI in Japanese type 2 diabetic patients.
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PMID:Metabolic syndrome, insulin resistance, and atherosclerosis in Japanese type 2 diabetic patients. 1761 56

The objective of this study was to assess the capacity of different criteria of metabolic syndrome (MetS) to identify risks of coronary heart diseases (CHDs) and related changes of adipocytokines in postmenopausal women. A cross-sectional study was carried out in 225 community-dwelling, elderly postmenopausal Chinese women (age, 66.77+/-5.09 years) without hormone replacement therapy (HRT). Baseline data such as blood pressure, body mass index (BMI), serum lipid profiles, and fasting glucose were analyzed, and insulin sensitivity was estimated via the homeostasis model assessment for insulin resistance. Serum tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), and adiponectin were measured simultaneously. The prevalence of MetS identified by the Third Report of the National Cholesterol Education Programme Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, the International Diabetes Federation (IDF), the Chinese Diabetes Society (CDS), and the Japanese Society of Internal Medicine (JPN) were 27.31%, 37.34%, 23.29%, and 13.65%, respectively. No significant differences of baseline data were found among different MetS groups, except for a significant higher waist circumference in the JPN-MetS group as compared with other MetS groups. The prevalence of confirmed CHD in the four MetS groups were 26.2%, 18.6%, 26.9%, and 32%, respectively. Odds ratios for CHD were 1.905 (95% CI=1.273-2.851), 1.208 (95% CI=0.778-1.876), 1.997 (95% CI=1.238-3.221), and 2.336 (95% CI=1.119-4.876), respectively. The JPN-MetS group had higher levels of TNFalpha and IL-6, whereas the CDS-MetS group correlated better with lower adiponectin levels. The IDF definition for MetS is the most sensitive one with regard to metabolic disorders, whereas JPN and CDS definitions correlate better with CHD and changes of adipocytokines among the four criteria studied.
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PMID:Risks of CHD identified by different criteria of metabolic syndrome and related changes of adipocytokines in elderly postmenopausal women. 1782 56

Adipocyte fatty acid-binding protein (A-FABP) has been reported to be increased in obese adults and to be related to metabolic syndrome. Because studies concerning A-FABP in weight loss are limited and studies in obese children are missing, we analyzed A-FABP in obese children before and after weight loss. Fasting serum A-FABP, leptin, insulin, glucose, triglycerides, low-and high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and tumor necrosis factor alpha concentrations as markers of the metabolic syndrome, and weight status (body mass index and percentage body fat based on skinfold measurements) were determined in 30 obese children (median age, 11.9 years) before and after participating in a 1-year obesity intervention. Furthermore, A-FABP levels were measured in 10 nonobese children of similar age, sex, and pubertal stage. Obese children had significantly (P < .001) higher A-FABP concentrations compared with nonobese children. In backward multivariate linear regression analysis, A-FABP correlated significantly (P < .05) with percentage body fat and leptin, but not with any of the markers of the metabolic syndrome. Changes of A-FABP concentrations correlated significantly with changes of percentage body fat (r = 0.53, P = .001) and leptin (r = 0.55, P < .001), but not with any changes of parameters of the metabolic syndrome. Substantial weight loss in 10 children led to a significant (P < .05) decrease in A-FABP levels in contrast to the 20 children without change of weight status. In cross-sectional as well as longitudinal analyses, A-FABP levels were related to weight status and leptin levels. Further longitudinal studies are necessary to study the relationship between A-FABP concentrations and parameters of the metabolic syndrome.
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PMID:Adipocyte fatty acid-binding protein in obese children before and after weight loss. 1799 29

Epidemiological studies have shown that, in psoriasis patients, associated disorders may occur more frequently than expected. Such comorbidities include psoriatic arthritis, psoriatic pustular diseases, Crohn disease, and signs of metabolic syndrome, which leads to atherosclerosis with coronary heart disease. Although the disorders represent separate entities, they appear to follow overlapping pathogenic pathways. Comorbidities often become clinically manifest years after onset of psoriasis and are frequently seen in severe disease. Persistent low-grade inflammation with secretion of proinflammatory cytokines (eg, tumor necrosis factor alpha) favors the development of insulin resistance and metabolic syndrome. In addition, biochemical and immunologic observations point toward an inflammatory immune mechanism that uses tools of the innate defense armamentarium.
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PMID:Comorbidities in psoriasis. 1802 89

Inflammation is associated with obesity, the metabolic syndrome, and diabetes. No data are available on the effect of weight reduction on the gene expression of cytokines in immune cells in obesity and the metabolic syndrome. We assessed how long-term weight loss affects expression of cytokines in peripheral blood mononuclear cells (PBMCs) in individuals with impaired glucose metabolism and the metabolic syndrome. Data from 34 subjects randomized to either a weight reduction or a control group for a 33-week period were analyzed. The messenger RNA (mRNA) expression of interleukins (ILs) in PBMCs was measured using real-time polymerase chain reaction. Measures of insulin and glucose metabolism (intravenous and oral glucose tolerance tests), body composition, and circulating adipokines and inflammatory markers were also assessed. Weight reduction resulted in a decrease in the mRNA expression of IL-1beta (IL1B), IL-1 receptor antagonist, and tumor necrosis factor alpha (P < .001) and an increase in expression of IL-6 (IL6) and IL-8 (P < .01). The increase in IL6 expression was associated with a decrease in fasting glycemia (r = -0.53, P < .01). Interestingly, the decrease in IL1B expression was correlated with an increase in insulin sensitivity index (r = -0.68, P < .01). In general, a decrease in circulating levels of adipokines and inflammatory markers was also observed after weight loss. Weight loss altered gene expression of cytokines related to inflammation and the immune response in PBMCs. Changes in IL6 mRNA expression were associated with changes in fasting glycemia. The decrease in IL-1 receptor antagonist expression after weight loss and the strong correlation between the decrease in IL1B expression and the increase in insulin sensitivity suggest a contribution of these genes to insulin-resistant states found in obesity and the metabolic syndrome.
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PMID:Effect of weight loss on cytokine messenger RNA expression in peripheral blood mononuclear cells of obese subjects with the metabolic syndrome. 1819 Oct 48

Metabolic syndrome, also known as the insulin resistance syndrome (IRS), dysmetabolic syndrome or syndrome X, is a burgeoning global epidemic. This constellation of risk factors, namely glucose intolerance, hypertension, dyslipidemia (high triglyceride and low HDL cholesterol), central obesity, pro-inflammatory and prothrombotic state, culminating to the development of premature cardiovascular and renal disease, has significant impact on life expectancy, societal productivity and quality of life. The underlying mechanism of this complex syndrome remains to be elucidated. In recent years, light has been shed on the roles of neuroendocrine system and adipocytokines on the pathogenesis of IRS. In this review, we summarize the possible links between insulin and various hormones (growth hormones (GH), catecholamines, glucocorticoids and sex hormones), partly mediated through visceral adiposity and adipocytokines (notably adiponectin, leptin, resistin, visfatin, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6)) in the pathogenesis of this syndrome.
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PMID:The role of adipocytokines and neurohormonal dysregulation in metabolic syndrome. 1822 Jun 44

Chronic infection with hepatitis C virus (HCV) can induce insulin resistance (IR) in a genotype-dependent fashion, thus contributing to steatosis, progression of fibrosis and resistance to interferon therapy. The molecular mechanisms in genotype 1 patients that lead to metabolic syndrome are still ambiguous. Based on our current understanding, HCV proteins associate with mitochondria and endoplasmic reticulum and promote oxidative stress. The latter mediates signals involving the p38 mitogen-activated protein kinase and activates nuclear factor kappa B. This transcription factor plays a key role in the expression of cytokines, tumor necrosis factor alpha (TNF-alpha), interleukin 6, interleukin 8, tumor growth factor beta, and Fas ligand. TNF-alpha inhibits the function of insulin receptor substrates and decreases the expression of the glucose transporter and lipoprotein lipase in peripheral tissues, which is responsible for the promotion of insulin resistance. Furthermore, reduced adiponectin levels, loss of adiponectin receptors, and decreased anti-inflammatory peroxisome proliferator-activated receptor alpha in the liver of HCV patients may contribute to reduced fatty acid oxidation, inflammation, and eventually lipotoxicity. This chain of events may be initiated by HCV-associated IR and provides a direction for future research in the areas of therapeutic intervention.
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PMID:Hepatitis C virus infection: molecular pathways to metabolic syndrome. 1875 83

Obesity promotes insulin resistance and chronic inflammation. Disrupting any of several distinct steps in lipid synthesis decreases adiposity, but it is unclear if this approach coordinately corrects the environment that propagates metabolic disease. We tested the hypothesis that inactivation of FAS in the hypothalamus prevents diet-induced obesity and systemic inflammation. Ten weeks of high-fat feeding to mice with inactivation of FAS (FASKO) limited to the hypothalamus and pancreatic beta cells protected them from diet-induced obesity. Though high-fat fed FASKO mice had no beta-cell phenotype, they were hypophagic and hypermetabolic, and they had increased insulin sensitivity at the liver but not the periphery as demonstrated by hyperinsulinemic-euglycemic clamps, and biochemically by increased phosphorylated Akt, glycogen synthase kinase-3beta, and FOXO1 compared with wild-type mice. High-fat fed FASKO mice had decreased excretion of urinary isoprostanes, suggesting less oxidative stress and blunted tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) responses to endotoxin, suggesting less systemic inflammation. Pair-feeding studies demonstrated that these beneficial effects were dependent on central FAS disruption and not merely a consequence of decreased adiposity. Thus, inducing central FAS deficiency may be a valuable integrative strategy for treating several components of the metabolic syndrome, in part by correcting hepatic insulin resistance and suppressing inflammation.
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PMID:Inactivation of hypothalamic FAS protects mice from diet-induced obesity and inflammation. 1902 18

Nonalcoholic fatty liver disease (NAFLD) and its advanced stage, nonalcoholic steatohepatitis (NASH), are the most common causes of chronic liver disease in the United States. NASH features the metabolic syndrome, inflammation, and fibrosis. Probiotics exhibit immunoregulatory and anti-inflammatory activity. We tested the hypothesis that probiotic VSL#3 may ameliorate the methionine-choline-deficient (MCD) diet-induced mouse model of NASH. MCD diet resulted in NASH in C57BL/6 mice compared to methionine-choline-supplemented (MCS) diet feeding evidenced by liver steatosis, increased triglycerides, inflammatory cell accumulation, increased tumor necrosis factor alpha levels, and fibrosis. VSL#3 failed to prevent MCD-induced liver steatosis or inflammation. MCD diet, even in the presence of VSL#3, induced up-regulation of serum endotoxin and expression of the Toll-like receptor 4 signaling components, including CD14 and MD2, MyD88 adaptor, and nuclear factor kappaB activation. In contrast, VSL#3 treatment ameliorated MCD diet-induced liver fibrosis resulting in diminished accumulation of collagen and alpha-smooth muscle actin. We identified increased expression of liver peroxisome proliferator-activated receptors and decreased expression of procollagen and matrix metalloproteinases in mice fed MCD+VSL#3 compared to MCD diet alone. MCD diet triggered up-regulation of transforming growth factor beta (TGFbeta), a known profibrotic agent. In the presence of VSL#3, the MCD diet-induced expression of TGFbeta was maintained; however, the expression of Bambi, a TGFbeta pseudoreceptor with negative regulatory function, was increased. In summary, our data indicate that VSL#3 modulates liver fibrosis but does not protect from inflammation and steatosis in NASH. The mechanisms of VSL#3-mediated protection from MCD diet-induced liver fibrosis likely include modulation of collagen expression and impaired TGFbeta signaling.
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PMID:VSL#3 probiotic treatment attenuates fibrosis without changes in steatohepatitis in a diet-induced nonalcoholic steatohepatitis model in mice. 1911 16


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