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)

Previous study showed that mulberry (Morus Alba L.) leaf (ML) ameliorates atherosclerosis in apoE(-/-) mice. Although the adipocytokine dysregulation is an important risk factor for atherosclerotic cardiovascular disease, the effect of ML on metabolic disorders related to adipocytokine dysregulation and inflammation has not been studied. Therefore, we studied the effects of ML in metabolic disorders and examined the mechanisms by which ML ameliorates metabolic disorders in db/db mice. We treated db/db mice with ML, pioglitazone, or both for 12 weeks and found that ML decreased blood glucose and plasma triglyceride. Co-treatment with ML and pioglitazone showed additive effects compared with pioglitazone. Moreover, their co-treatment attenuated the body weight increase observed under the pioglitazone treatment. ML treatment also increased the expression of adiponectin, and decreased the expression of TNF-alpha, MCP-1, and macrophage markers in white adipose tissue (WAT). Furthermore, ML decreased lipid peroxides and the expression of NADPH oxidase subunits in WAT and liver. Their co-treatment enhanced these effects. Thus, ML ameliorates adipocytokine dysregulation at least in part through inhibiting oxidative stress in WAT of db/db mice, and that ML may be a basis for a pharmaceutical for the treatment of the metabolic syndrome as well as reducing adverse effects of pioglitazone.
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PMID:Mulberry leaf ameliorates the expression profile of adipocytokines by inhibiting oxidative stress in white adipose tissue in db/db mice. 1907 Aug 57

Inflammatory and redox signals could render lamellar tissue susceptible to damage and contribute to higher risk for laminitis in obese or insulin resistant ponies just as these factors contribute to health risks in humans with metabolic syndrome. This study evaluated circulating markers of inflammatory and redox status in ponies that had a history of recurrent bouts of pasture-associated laminitis (PL, n = 42) or had never developed clinical laminitis (NL, n = 34) under the current management conditions. There were no differences (P > 0.05) between PL and NL ponies for markers of antioxidant function (glutathione, glutathione peroxidase, superoxide dismutase) or increased oxidative pressure (malondialdehyde, apoptosis, 3-nitrotyrosine). Inflammatory status, as indicated by fibrinogen concentration, was also not different between pony groups (P = 0.84). However, PL ponies had higher (P < 0.001) plasma concentrations of the pro-inflammatory cytokine TNF-alpha than NL ponies. This suggests that a predisposition to laminitis is associated with increased circulating inflammatory cytokines. TNF-alpha could also represent a contributing factor to increased insulin resistance observed in laminitis prone ponies. These results provide new insight into potential mechanisms and risk factors underlying laminitis.
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PMID:Inflammatory and redox status of ponies with a history of pasture-associated laminitis. 1910 99

Cardiovascular diseases and type 2 diabetes are the major causes of mortality in Mexico. Metabolic syndrome (MS) is a cluster of factors that increase the risk to develop such diseases. Previous studies have shown that MS is associated with high tumor necrosis factor (TNF-alpha) levels. In fact, TNF-alpha has been proposed to be a useful marker for clinical diagnosis of inflammation at an early stage. Therefore, we analyzed TNF-alpha concentrations in Mexican individuals with or without MS and related these levels to the associated MS components. Clinical, anthropometric, and biochemical data were analyzed in 41 healthy and 39 MS individuals. Individuals were similarly grouped by age and gender.The serum TNF-alpha levels measured by a highly sensitive enzyme-linked immunosorbent assay (ELISA) kit were increased significantly in MS subjects compared with healthy individuals (P<0.001). The assay showed 78.1% sensitivity and 61.5% specificity with a cut-point level of 1.36 pg/mL. TNF-alpha levels higher than the cut-point value were correlated with insulin resistance indices. These findings support the hypothesis that serum TNF-alpha concentration could be a useful marker for early MS diagnosis. Nevertheless, we suggest the establishment of specific cut-point values in each studied population to evaluate potential clinical applications.
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PMID:Establishment of a cut-point value of serum TNF-alpha levels in the metabolic syndrome. 1914 Feb 12

Angiotensin II suppresses the insulin sensitivity via enhancement of serine phosphorylation of insulin receptor and suppression of tyrosine phosphorylation of IRS-1. Adiponectin increases insulin sensitivity, and TNF-alpha decreases insulin sensitivity. From our studies, the suppressed adiponectin and increased TNF-alpha may play an important role of the insulin resistance mechanisms. Angiotensin II suppresses the differentiation of adipocyte. Large sized adipocytes increase TNF-alpha and decrease adiponectin. Angiotensin II also has the direct stimulating action on TNF-alpha synthesis. ARB increases adiponectin a nddecreases TNF-alpha. Improvements of these adipocytokines dysfunction by ARB may concern tothe improvement of insulin resistance. The significance of various adipocytokines in insulin resistance and metabolic syndrome is also introduced.
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PMID:[Metabolic syndrome]. 1934 41

Regular consumption of flavonoids may reduce the risk for CVD. However, the effects of individual flavonoids, for example, quercetin, remain unclear. The present study was undertaken to examine the effects of quercetin supplementation on blood pressure, lipid metabolism, markers of oxidative stress, inflammation, and body composition in an at-risk population of ninety-three overweight or obese subjects aged 25-65 years with metabolic syndrome traits. Subjects were randomised to receive 150 mg quercetin/d in a double-blinded, placebo-controlled cross-over trial with 6-week treatment periods separated by a 5-week washout period. Mean fasting plasma quercetin concentrations increased from 71 to 269 nmol/l (P < 0.001) during quercetin treatment. In contrast to placebo, quercetin decreased systolic blood pressure (SBP) by 2.6 mmHg (P < 0.01) in the entire study group, by 2.9 mmHg (P < 0.01) in the subgroup of hypertensive subjects and by 3.7 mmHg (P < 0.001) in the subgroup of younger adults aged 25-50 years. Quercetin decreased serum HDL-cholesterol concentrations (P < 0.001), while total cholesterol, TAG and the LDL:HDL-cholesterol and TAG:HDL-cholesterol ratios were unaltered. Quercetin significantly decreased plasma concentrations of atherogenic oxidised LDL, but did not affect TNF-alpha and C-reactive protein when compared with placebo. Quercetin supplementation had no effects on nutritional status. Blood parameters of liver and kidney function, haematology and serum electrolytes did not reveal any adverse effects of quercetin. In conclusion, quercetin reduced SBP and plasma oxidised LDL concentrations in overweight subjects with a high-CVD risk phenotype. Our findings provide further evidence that quercetin may provide protection against CVD.
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PMID:Quercetin reduces systolic blood pressure and plasma oxidised low-density lipoprotein concentrations in overweight subjects with a high-cardiovascular disease risk phenotype: a double-blinded, placebo-controlled cross-over study. 1940 38

Heme oxygenase (HO) and cytochrome P450 (P450)-derived epoxyeicosatrienoic acids (EETs) participate in vascular protection, and recent studies suggest these two systems are functionally linked. We examined the consequences of HO deficiency on P450-derived EETs with regard to body weight, adiposity, insulin resistance, blood pressure, and vascular function in HO-2-null mice. The HO-2-null mice were obese, displayed insulin resistance, and had high blood pressure. HO-2 deficiency was associated with decreases in cyp2c expression, EET levels, HO-1 expression, and HO activity and with an increase in superoxide production and an impairment in the relaxing response to acetylcholine. In addition, HO-2-null mice exhibited increases in serum levels of tumor necrosis factor (TNF)-alpha and macrophage chemoattractant protein (MCP)-1 and a decrease in serum adiponectin levels. Treatment of HO-2-null mice with a dual-activity EET agonist/soluble epoxide hydrolase inhibitor increased renal and vascular EET levels and HO-1 expression, lowered blood pressure, prevented body weight gain, increased insulin sensitivity, reduced subcutaneous and visceral fat, and decreased serum TNF-alpha and MCP-1, while increasing adiponectin and restoring the relaxing responses to acetylcholine. The decrease in cyp2c expression and EETs levels in HO-2-null mice underscores the importance of the HO system in the regulation of epoxygenase levels and suggests that protection against obesity-induced cardiovascular complications requires interplay between these two systems. A deficiency in one of these protective systems may contribute to the adverse manifestations associated with the clinical progression of the metabolic syndrome.
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PMID:Epoxyeicosatrienoic acid agonist rescues the metabolic syndrome phenotype of HO-2-null mice. 1971 90

It has been reported that prenatal immune stress induced by lipopolysaccharides or cytokines increases food intake and leads to obesity and other features of metabolic syndrome in adulthood. Using Sprague-Dawley rats, we evaluated whether neonatal LPS injection altered their body weight regulation systems under non-stress and immune stress conditions. On Day 10 after birth, all pups were injected with LPS (100 microg/kg, i.p.) (PND(10)LPS) or saline (PND(10)Saline). After weaning, body weight was significantly elevated in PND(10)LPS compared with PND(10)Saline. Thereafter, the rats were injected with LPS (100 microg/kg, i.p.) or saline (used as a basal condition) from 7 to 8 weeks of age. Under basal conditions, cumulative food intake were significantly higher, serum leptin concentration was significantly increased, and hypothalamic NPY mRNA expression was significantly decreased in PND(10)LPS compared with PND(10)Saline. Under adult LPS injected conditions, body weight gain and cumulative food intake were suppressed in both the PND(10)LPS and PND(10)Saline groups compared with those observed under basal adult saline-injected conditions. The suppressive effects induced by adult LPS injection were less evident in the PND(10)LPS group than in the PND(10)Saline group. Adult LPS injection increased the serum leptin concentration in the PND(10)Saline rats, but not in the PND(10)LPS rats. In addition, adult LPS injection increased the mRNA expression of anorexinergic factors (IL-1beta, and TNF-alpha), and decreased that of the orexinergic factor NPY in both groups. However, the influence of adult LPS injection upon these factors was less evident in the PND(10)LPS group than in the PND(10)Saline group. These results suggest that neonatal LPS injection alters body weight regulation under both non-stress and immune stress conditions in male rats. Changes in the endocrine, neuropeptide, and cytokine regulation systems might be involved in these alterations.
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PMID:Neonatal LPS injection alters the body weight regulation systems of rats under non-stress and immune stress conditions. 1973 50

Non-alcoholic fatty liver disease (NAFLD) has recently been recognized as a leading cause of abnormal liver function tests. Its spectrum ranges from simple steatosis, which is usually a benign and non progressive condition, to non-alcoholic steatohepatitis (NASH), which may progress to cirrhosis and hepatocellular carcinoma. NASH is thought to be almost 10% of NALFD and part of metabolic syndrome. NASH patients usually have insulin resistance, frequently combined with hypertension, hyperlipidemia and diabetes. The etiology of NASH remains unclear, but most investigators agree that the development of NASH requires underlying steatosis followed by a "second hit" that induces inflammation, fibrosis, or necrosis. The interaction of adipocytokines (TNF-alpha, adiponectin) with oxidative stress and lipid peroxidation has been postulated to play a key role in NASH. The basic therapy for NASH is an improved of lifestyle, including exercise and diet. Drug therapy should be considered as additional therapy.
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PMID:[Diagnosis and therapy in NASH]. 1986 Feb 10

Nonalcoholic steatohepatitis (NASH) represents one of the most common liver diseases. It is strongly associated with obesity and insulin resistance and is thought to be part of the metabolic syndrome. NASH can progress to cirrhosis and liver failure. Adipohormones, synthesized in adipose tissue, are involved in the pathophysiology of many acute and chronic liver diseases. The aim of this study was to evaluate the plasma concentrations of adiponectin, resistin, leptin, TNF-alpha and Il-6 in patients with NASH, as well as their correlation with the pathologic parameters. Serum concentration of leptin, adiponectin, resistin, insulin, TNF-alpha, IL-6 were measured with ELISA method. Liver biopsies were obtained from 18 (age 42.55+/-21 years) patients. NASH has been classified according to Dixon score. The control group was represented by 16 non-obese subjects. Mean serum concentration of adiponectin in patients with NASH was significantly lower than in healthy subjects (4.87+/-1.96 vs. 8.33+/-4.56 ng/ml; p<0.05). Mean serum levels of TNF-alpha in patients with NASH were significantly higher than in controls (34.2+/-19.7 vs. 20.7+/-15.5 ng/ml; p<0.05). In patients with more advanced inflammation (grade 2-3) and fibrosis (stage 2) in pathology, serum concentration of leptin was significantly higher than in patients with steatosis and less advanced inflammation (grade 1) and fibrosis (stage 1) (median 8.94 vs. 16.2 ng/ml; p<0.05). No significant differences of serum concentration of others adipohormones between these two groups of patients were stated. Moreover, we observed the correlation in serum levels (examined group vs controls) between: resistin and TNF-alpha (r = 0.62; p<0.05), adiponectin and IL-6 (r = -0.60; p<0.05) and leptin and insulin (r = -0.51; p<0.05). In conclusion, based on our study we speculate that changes of adipohormones levels may be markers of NASH and the serum level of leptin can be associated with more advanced form of NASH.
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PMID:Adipohormones as prognostric markers in patients with nonalcoholic steatohepatitis (NASH). 1999 85

Circulating levels of inflammatory and prothrombotic factors are elevated in the metabolic syndrome (MS) and linked with the occurrence of cardiovascular events. The aim of our study was to investigate the relationship between inflammatory and prothrombotic markers and the MS in elderly institutionalized residents. A total of 326 non-diabetic residents of Chuang-Hua Veterans Care Home (age: 79.9+/-4.1 years; 100% males) were enrolled. MS was diagnosed according to the AHA/NHLBI Scientific Statement criteria. Body fat percentage was measured by bioelectrical impedance analysis. Insulin resistance was calculated by homeostasis model assessment for insulin resistance (HOMA-IR). Inflammatory markers, including tumor necrosis factor-a (TNF-alpha), high sensitivity C-reactive protein (hsCRP), and plasminogen activator inhibitor-1 (PAI-1), were determined using ELISA. Elderly residents with the MS had higher systolic and diastolic blood pressures (both p < 0.001) and higher HOMA-IR (p < 0.001), hsCRP (p = 0.008), and PAI-1 levels (p < 0.001) than those without the MS. On multivariate logistic regression analysis, PAI-1 was an independent risk factor for the MS. Of the MS components, elderly residents with higher waist circumferences and higher levels of plasma fasting glucose, and triglyceride (TG), and lower levels of high density lipoprotein (HDL) had higher PAI-1 levels than those without the above components.
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PMID:Plasminogen activator inhibitor type 1 (PAI-1) is a valuable biomarker for predicting the metabolic syndrome (MS) in institutionalized elderly residents in Taiwan. 2000 26


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