Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study were to answer the question 1.) Whether circulating pro-inflammatory markers of endothelial dysfunction and due to chronic low-grade inflammation of obesity, are altered in untreated lean, young relatively healthy polycystic ovary syndrome (PCOS) patients in comparison with healthy controls; 2.) Whether postprandial plasma concentration pattern of ghrelin and PYY can be predictable as risk factors for atherosclerosis and depend of obesity. Forty young women with PCOS were divided in two groups: 19 lean and 21 obese. The control group included 20 lean, healthy volunteers. Plasma total and active ghrelin, total PYY and PYY(3-36), serum adiponectin and insulin were measured using RIA technique, serum sCD40L, visfatin, sP-, sE-selectins, resistin by EIA. Composition of test meal was: 527 kcal total and consisted of 24.1% fat, 54.4% carbohydrate and 21.5% protein. Total and active ghrelin and total PYY were significantly lower in obese PCOS women, whereas active ghrelin was also significantly lower in lean PCOS women compared to controls. Postprandial plasma total ghrelin levels decrease were blunted in lean and obese compared to controls (12.8 % and 18.2% vs 28.2 %). Postprandial plasma active ghrelin decreased in lean and obese PCOS groups (49.9 % and 44.1 %) and controls (63.8 %). PCOS subjects exhibited smaller rises in postprandial levels of total PYY. Postprandial plasma PYY(3-36) levels increased in obese PCOS women (30.9 %) and controls (41%), whereas lean PCOS women exhibited blunted increase (11.5%). sCD40L levels increased, whereas adiponectin decreased in PCOS groups independently, whereas rise in visfatin, sE- and sP-selectin and the fall in adiponectin was associated with obesity. sP- and sE -selectins correlated positively with obesity. In summary, our study provides the first evidence that lean untreated young PCOS women contribute to the so called "pancreatic islet adaptation to insulin resistance" because of ghrelin and PYY profiles. We confirmed existing of low-grade chronic inflammation in early stage of visceral obesity in lean PCOS patients. The lost endogenous "islet adaptation to insulin resistance" may lead to endothelial dysfunction and promote acceleration of atherosclerosis.
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PMID:Postprandial response of ghrelin and PYY and indices of low-grade chronic inflammation in lean young women with polycystic ovary syndrome. 1881 36

The effects of estrogen replacement therapy (ERT) to cardiovascular disease risk are still unclear. Low adiponectin and high resistin plasma concentrations are reported to be associated with atherosclerosis. However, it is not known how ERT affects plasma adiponectin and resistin concentrations. Seventy-three hysterectomized, nondiabetic, postmenopausal women were randomized in a double-blind, double-dummy study to receive either peroral estradiol valerate or transdermal 17beta-estradiol gel for 6 months. Biochemical measurements were determined from samples taken before and after the therapy. Peroral estradiol valerate therapy decreased adiponectin concentrations from 13.6 to 11.6 mg/L (P = .008), whereas transdermal 17beta-estradiol gel had no effect (12.7 vs 12.2 mg/L). Neither treatment changed the resistin concentrations significantly. Plasma concentrations of estradiol and estrone did not correlate with adiponectin or resistin concentrations before or after therapy. The change in adiponectin concentration correlated significantly with the changes in waist-hip ratio, very low-density lipoprotein triglycerides, and insulin-like growth factor 1 in the peroral estradiol valerate group. The changes in these variables and the change in estradiol concentration explained 43.1% (P = .001) of the variability in the change of plasma adiponectin, the change in very low-density lipoprotein triglycerides being the strongest determinant (beta = -.407, P = .011). The results show that peroral ERT can decrease plasma adiponectin levels. However, ERT does not seem to influence plasma resistin concentrations.
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PMID:Estrogen replacement therapy decreases plasma adiponectin but not resistin in postmenopausal women. 1894 Mar 87

Obesity is associated with an array of health problems in adult and pediatric populations. Understanding the pathogenesis of obesity and its metabolic sequelae has advanced rapidly over the past decades. Adipose tissue represents an active endocrine organ that, in addition to regulating fat mass and nutrient homeostasis, releases a large number of bioactive mediators (adipokines) that signal to organs of metabolic importance including brain, liver, skeletal muscle, and the immune system--thereby modulating hemostasis, blood pressure, lipid and glucose metabolism, inflammation, and atherosclerosis. In the present review, we summarize current data on the effect of the adipose tissue-derived hormones adiponectin, chemerin, leptin, omentin, resistin, retinol binding protein 4, tumor necrosis factor-alpha and interleukin-6, vaspin, and visfatin on insulin resistance.
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PMID:Adipokines and insulin resistance. 1900 16

Hyperplasia and hypertrophy of fat cells can be found in obesity and increased adiposity is associated with endothelial dysfunction as an early event of atherosclerosis. However, it is unclear whether human adipocytes directly influence endothelial protein secretion. To study the crosstalk between fat and endothelial cells, human umbilical venous endothelial cells (HUVECs) were cultured in infranatants (Adipo) of primary differentiated human adipocytes. Interestingly, significantly increased secretion of 23 cytokines and chemokines from HUVECs was detected in four independent experiments after Adipo stimulation by protein array analysis detecting a total of 174 different proteins. Among those, time-dependent Adipo-induced upregulation of cytokine secretion in HUVECs was confirmed by ELISA for interleukin (IL)-8, monokine induced by gamma interferon, macrophage inflammatory protein (MIP)-1beta, MIP-3alpha, monocyte chemoattractant protein-1, and IL-6. Factors besides adiponectin, leptin, resistin, and tumor necrosis factor alpha appear to mediate these stimulatory effects. Our findings suggest that endothelial cell secretion is significantly influenced towards a proinflammatory pattern by adipocyte-secreted factors.
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PMID:Secretory products from human adipocytes stimulate proinflammatory cytokine secretion from human endothelial cells. 1917 2

The recent increase in the prevalence of obesity has significant contribution to development of atherosclerosis and consequent cardiovascular disease. Obesity especially visceral obesity causes insulin resistance and is associated with dyslipidemia, impaired glucose metabolism, and hypertension, all of which exacerbate atherosclerosis. One plausible mechanism proposed recently is that factors known as adipocytokines, produced by adipose tissue in obesity can directly impact the atherogenic environment of the vessel wall by regulating gene expression and function in endothelial, arterial smooth muscle, and macrophage cells. These include TNFalpha, leptin, adiponectin, resistin, MCP1 and PAIl as well as free fatty acids. Reduction of visceral fat mass leads to amelioration of these risk factors and potentially prevents cardiovascular events.
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PMID:[Obesity and atherosclerosis]. 1920 8

Resistin, a newly discovered protein, promotes endothelial dysfunction and proinflammatory activation, contributing to subclinical atherosclerosis in different clinical settings. In this study we sought to investigate the relationship of increased resistin levels with estimated glomerular filtration rate (eGFR), the most established marker of kidney impairment, in hypertensive subjects. Our population consisted of 132 untreated non-diabetic subjects with stage I-II essential hypertension (49 males, mean age=54 years, office blood pressure (BP)=159/100 mm Hg). In all patients eGFR was assessed by the Modification in Renal Disease equation and venous blood sampling was performed for estimation of resistin concentrations. The distribution of resistin was split by the median (4.63 ng ml(-1)) and accordingly subjects were stratified into those with high and low values. Hypertensive patients with high (n=66) compared to those with low resistin (n=66) exhibited lower eGFR values (77.1+/-9.4 vs 89.1+/-12.2 ml min(-1) per 1.73m(2), P<0.0001), even after adjustment for established confounders. In the total population, resistin was associated with 24-h systolic BP (r=0.244, P<0.05), serum creatinine (r=0.311, P=0.007) and eGFR (r=-0.519, P<0.0001). Multiple regression analysis revealed that age (b=0.379, P=0.01), body mass index (b=0.158, P=0.022), 24-h systolic BP (b=0.284, P=0.006) and resistin (b=0.429, P<0.0001) were independent predictors of eGFR (R(2)=0.436, P<0.0001). In essential hypertensive subjects, higher resistin levels are associated with renal function impairment, as reflected by decreased eGFR. Moreover, the independent association of resistin with eGFR suggests involvement of resistin in the progression of kidney damage in the early stages of hypertension.
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PMID:Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension. 1926 83

Resistin, which appears to be related to insulin resistance, is secreted mainly from macrophages in human and some of its polymorphisms have been reported. Based on recent in vitro studies, resistin may be associated with atherosclerosis by mediating endothelial hyperactivity. We investigated whether resistin polymorphism at -420C>G is associated with serum resistin levels and diabetic macroangiopathy (coronary heart disease, arteriosclerosis obliterans, and stroke) in 349 Japanese type 2 diabetic patients (DM) and 286 non-diabetic controls (non-DM). Serum resistin levels in DM with a history of stroke were significantly higher than those without, 19.6+/-2.1 and 12.4+/-0.5 ng/ml (P<0.001), respectively. Furthermore, the levels were significantly increased in a genotype-dependent manner (CC, CG, GG) based on the polymorphism at -420C>G (P<0.001) in both DM and non-DM. The prevalence of stroke in DM significantly increased according to the presence of mutations (P<0.035). In multivariate logistic-regression analysis, individuals with the CG or GG genotypes were significantly more likely to have had a stroke than individuals with the CC genotype (vs. CG; OR 2.99, P=0.024, vs. GG; OR 4.49, P=0.010). These data suggested that the genotyping of resistin polymorphism at -420(C>G) can be a risk marker for stroke susceptibility in Japanese type 2 diabetic patients.
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PMID:Polymorphism in resistin promoter region at -420 determines the serum resistin levels and may be a risk marker of stroke in Japanese type 2 diabetic patients. 1926 54

Resistin is a potential link between obesity and insulin resistance or type 2 diabetes. In rodents, resistin is primarily expressed in and secreted from mature adipocytes, with some expression in pancreatic islets and portions of the pituitary and hypothalamus. Its secretion can be up-regulated by several factors, including insulin and glucose. The exposure of rodents, or their cells, to resistin results in decreased response to insulin. This is likely in part due to an up-regulation of suppressor of cytokine signaling (SOCS)-3, which interferes with the activation of insulin receptor substrate (IRS)-1. However, in humans resistin is expressed primarily by macrophages and seems to be involved in the recruitment of other immune cells and the secretion of pro-inflammatory factors, including tumor necrosis factor (TNF)alpha. Human resistin may interfere with insulin signaling by stimulating the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which dephosphorylates 3-phosphorylated phosphoinositide (PIP(3)). Resistin also seems to be involved in the development of atherosclerosis in humans by promoting the formation of foam cells and the proliferation and migration of vascular endothelial and smooth muscle cells. Many of the inflammatory related functions of human resistin appear to be regulated by activation of the nuclear factor (NF)kappaB transcription factor. The divergent roles of resistin in humans and rodents are evident by the data presented in this review but they will not be able to be fully understood until the resistin receptor is identified.
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PMID:Role of resistin in insulin sensitivity in rodents and humans. 1927 76

Altered levels of adipokines, derived as a result of distorted adipocytes, are the major factors responsible for changing biochemical parameters in obesity that leads to the development of metabolic disorders such as insulin resistance and atherosclerosis. In our previous reports, chitosan oligosaccharides (CO) were proved to inhibit the differentiation of 3T3-L1 adipocytes. In the present study, an attempt was made to investigate the anti-obesity and anti-diabetic effect of CO on ob/ob mice, by means of differential proteomic analysis of plasma. This was followed by immunoblotting, and gene expression in adipose tissue to clarify the molecular mechanism. CO treatment showed reduced diet intake (13%), body weight gain (12%), lipid (29%) and glucose levels (35%). 2-DE results showed differential levels of five proteins namely RBP4, apoE, and apoA-IV by >2-fold down-regulation and by >2-fold of apoA-I and glutathione peroxidase (GPx) up-regulation after CO treatment. Immunoblotting studies of adiponectin and resistin showed amelioration in their levels in plasma. Furthermore, the results of gene expressions for adipose tissue specific TNF-alpha, and IL-6 secretary molecules were also down-regulated by CO treatment. Gene expressions of PPAR gamma in adipose tissue were in good agreement with the ameliorated levels of adipokines, thereby improving the pathological state. Taken together, CO might act as a potent down-regulator of obesity-related gene expression in ob/ob mice that may normalize altered plasma proteins to overcome metabolic disorders of obesity.
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PMID:Plasma proteome analysis for anti-obesity and anti-diabetic potentials of chitosan oligosaccharides in ob/ob mice. 1929 49

In addition to its role as an energy storage depot, adipose tissue is now recognized as a complex endocrine organ. Adipose tissue releases a variety of factors, termed adipokines, that regulate energy metabolism, cardiovascular function, reproductive status, and immune function. Some of the better-studied adipokines include leptin, adiponectin, and components of the renin-angiotensin system such as angiotensinogen. The function of more recently discovered adipokines such as resistin are under intense scrutiny. Abnormal production or regulation of adipokines occurs in obese individuals and is implicated in the development of a variety of associated co-morbidities including metabolic syndrome, type 2 diabetes, atherosclerosis, heart disease, and cancer in people, although evaluation in domestic species is just beginning. Adipokines are now being examined as potential biomarkers for risk assessment for development of complications related to obesity. This article summarizes the function and regulation of some better-characterized adipokines. It also reviews the current information on the characterization of adipokines in some domestic species in which rates of obesity and obesity-related disorders are increasing, such as the dog, cat, and horse.
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PMID:Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. 1939 60


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