Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome refers to the clustering of upper body obesity, atherogenic dyslipidemia, insulin resistance and elevated blood pressure. Both, obesity and metabolic syndrome, have the potential to influence on the incidence and severity of cardiovascular disease with serious implications for worldwide health care systems. Obesity plays a central role in the development of insulin resistance and dyslipidemia through the mediation of a pro-inflammatory and pro-thrombotic state. Adipose tissue has been shown to exert important endocrine and immune functions. Pathogenesis of obesity associated metabolic syndrome is mediated by disturbed production and release of biologically active molecules by fat cells and other cells infiltrating fat tissue. In obese subjects synthesis of several bioactive compounds--adipokines and cytokines/chemokines by adipose tissue cells is dysregulated. Those bioactive molecules participate in regulation of apetite and energy homeostasis, lipid metabolism (tumour necrosis factor alpha--TNF-alpha), insulin sensitivity (TNF-alpha, adiponectin, resistin, visfatin) immunity (monocyte chemoattractant protein-1--MCP-1, TNF-alpha, IL-6), angiogenesis, blood pressure and hemostasis (plasminogen activator inhibitor--PAI-1). The effects of major pro-/anti-inflammatory and pro-thrombotic adipokines on several physiological processes will be discussed in this review. Also, an evidence-based approach to the laboratory diagnosis and treatment of metabolic syndrome will be presented.
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PMID:Markers of pro-inflammatory and pro-thrombotic state in the diagnosis of metabolic syndrome. 1821 26

Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome. Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body. This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process. Therefore, excessive fat mass may trigger metabolic and hemostatic disturbances as well as CVD. Adipocytokines may act locally or distally as inflammatory, immune or hormonal signalers. In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue. Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area.
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PMID:The new adipose tissue and adipocytokines. 1822 Jun 14

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

5'AMP-activated protein kinase (AMPK) is a serine/threonine kinase that acts as a fuel gauge in regulating energy metabolism. It restores cellular ATP levels by switching on catabolic pathways and switching off anabolic pathways. Some evidence indicates that AMPK could be also implicated in reproductive functions such as granulosa cell steroidogenesis and nuclear oocyte maturation in several species. Some metabolic hormones such as leptin, resistin, adiponectin (three adipokines) and ghrelin may in part act through the AMPK signaling. These hormones are also involved in the control of the reproductive functions at the hypothalamus-pituitary-gonadal axis level in both male and female. Thus, AMPK could be one of the signaling pathways controlling the interactions between energy balance and reproduction. The reproductive system is tightly coupled with energy balance, and thereby metabolic abnormalities can lead to the development of some physiopathological situations such as the polycystic ovary syndrome (PCOS). Women with PCOS show altered fertility mostly associated with metabolic disorders such as insulin-resistance, hyperinsulinemia and/or dyslipidemia. Metformin, an insulin-sensitizer, is used for the treatment of women with PCOS. It restores subnormal fertility and energy balance. Recent studies show that AMPK is involved in the mechanism of action of metformin. Thus, it may be a therapeutic target. However, further investigations are necessary to elucidate the functions of AMPK in both metabolic and reproductive tissues.
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PMID:[AMPK: a link between metabolism and reproduction?]. 1833 79

An increased amount of adipose tissue or its disproportionate distribution between central and peripheral body regions is related to the development of insulin resistance, type 2 diabetes mellitus, dyslipidemia, atherosclerosis, and coronary artery disease. Until recently, adipose tissue was regarded as a storage depot for lipids. It is now viewed as a hormonally active organ that plays a crucial metabolic role. The most important products of adipose tissue collectively referred to as adipocytokines, include adiponectin, leptin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), resistin, plasminogen-activating inhibitor-I (PAI-1), and angiotensinogen. These low and medium molecular weight proteins play an important role in the adipose tissue physiology and are believed to be a link between obesity, insulin resistance and endothelial dysfunction. This review describes the metabolic role of two of these proteins, adiponectin and leptin, in relation to insulin sensitivity.
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PMID:Adiponectin and leptin in relation to insulin sensitivity. 1837 Jun 42

The aim of present study was to identify the visceral adipose tissue genes differentially expressed in a well-characterized rat model of high-fat diet (HFD)-induced obesity. Male Sprague-Dawley rats were fed either the HFD (17 g lard + 3 g corn oil/100 g) or the normal diet (5 g corn oil/100 g) for 9 weeks. The HFD rats weighed 55% more and accumulated 85% to 133% greater visceral fats than did the normal-diet rats (P < .05). Animals given the HFD for 9 weeks acquired dyslipidemia, fatty liver, insulin resistance, and hyperleptinemia along with the overexpression of several obesity-related genes, such as leptin, tumor necrosis factor alpha, resistin, peroxisome proliferator-activated receptor gamma2, CCAAT/enhancer-binding protein alpha, and sterol regulatory element-binding protein-1c, in the epididymal adipose tissue. The differential gene expression profile obtained from the cDNA microarray analysis followed by the real-time polymerase chain reaction confirmation led to a recruitment of several uncharacterized adipose tissue genes responding to the HFD. We report herein, for the first time, that a series of genes which might be implicated in the insulin-stimulated glucose transporter 4 translocation, such as protein phosphatase 2 (formerly 2A), cell division cycle 42-interacting protein 4, syntaxin 6, linker of T-cell receptor pathways 10, as well as the genes which might be involved in cancer development, such as heat shock 10-kd protein 1, and ras-related C3 botulinum toxin substrate 1, were differentially expressed in the epididymal adipose tissue of rats rendered obese by an HFD.
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PMID:Genes are differentially expressed in the epididymal fat of rats rendered obese by a high-fat diet. 1908 40

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

Our aims were to evaluate the serum adiponectin and resistin levels at fasting and after glucose load and their interaction with risk of cardiovascular disease (CVD) in adolescents with polycystic ovary syndrome (PCOS). Twenty-two adolescents with PCOS and 16 healthy controls were included in the study. Oral glucose tolerance test (OGTT) was performed in all adolescents. Fasting lipids was measured. Insulin, glucose, adiponectin, and resistin levels were measured at 0 and 120 min of OGTT. Homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin-sensitivity check index (QUICKI), fasting glucose-to-insulin ratio (FGIR), and the whole -body insulin sensitivity index (ISI) were calculated. Fasting adiponectin was correlated with ISI (r = 0.729, p < 0.0001), FGIR (r = 0.696, p < 0.0001), QUICKI (r = 0.592, p = 0.004) and HDL-C (r = 0.516, p = 0.028), systolic blood pressure (r = -0.732, p < 0.0001), body mass index (r = -0.738, p < 0.0001), waist circumference (r = -0.706, p < 0.0001), and HOMA-IR (r = -0.595, p = 0.003). No correlation was found between resistin and insulin resistance indexes. Obese adolescents with PCOS have increased CVD risk such as dyslipidemia, hypertension, and insulin resistance than normo-weight PCOS. Hypoadiponectinaemia could be increase risks levels in obese girls with PCOS.
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PMID:Adiponectin and resistin concentrations after glucose load in adolescents with polycystic ovary syndrome. 1963 97

White adipose tissue is an endocrine organ producing numerous proteins known as adipokines, which include leptin, adiponectin, resistin, visfatin, and other factors, which are involved in most metabolic disorders. In obesity, plasma leptin concentrations are high due to leptin resistance that may result from the attenuation of leptin signaling in the hypothalamus. Leptin acts to inhibit appetite, stimulate thermogenesis, enhance fatty acid oxidation, decrease glucose, and reduce body weight, and fat. A reduced adiponectin level has been associated with insulin resistance, dyslipidemia, and atherosclerosis, and its low level is a predictor of later development of type 2 diabetes. Resistin expression is low in adipose tissue and high in bone marrow and lungs, its role in glucose homeostasis remains controversial, it has been associated with insulin resistance and obesity. Visfatin is a secretory protein highly enriched in visceral adipocytes, liver, muscle, and lymphocytes. An increase of visfatin levels in obesity was related to preservation of insulin sensitivity, it enhances glucose uptake by adipocytes and inhibits hepatocyte glucose release, it induces tyrosine phosphorylation, and interacts with insulin receptors. Many studies are still being conducted to highlight the role of adipokines in metabolic disorders.
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PMID:Adipokines and etiopathology of metabolic disorders. 1975 Feb 55

Because of methodological limitations and conflicting results of studies conducted thus far, the possible involvement of human adipose tissue in pleiotropic effects of statins and fibrates requires better understanding. Samples of visceral and subcutaneous adipose tissue obtained from 23 mixed dyslipidemic patients and 23 normolipidemic subjects were treated in vitro for 48 h with atorvastatin, fenofibric acid or both these agents. Visceral and subcutaneous fat of mixed dyslipidemic patients released more leptin, resistin, interleukin-6, tumor necrosis factor alpha (TNFalpha and plasminogen activator inhibitor-1 (PAI-1), and less adiponectin than respective adipose tissue of patients without lipid abnormalities. In both groups of patients, visceral and subcutaneous tissue varied in the amount of secreted adipokines. In dyslipidemic patients both drugs administered alone affected adipose tissue adiponectin and resistin secretion. Additionally, atorvastatin decreased PAI-1 while fenofibric acid reduced leptin release. A combined administration of atorvastatin and fenofibric acid changed the release of all studied markers by visceral fat but did not affect interleukin-6 and TNFalpha release by subcutaneous tissue. In normolipidemic subjects the effect on adipokine release was more pronounced in visceral fat, in which it was strongest if the drugs were given together. Adipose tissue hormonal activity differs between mixed dyslipidemic and normolipidemic patients and between visceral and subcutaneous adipose tissue. Atorvastatin and fenofibrate exhibit their pleiotropic effects in part by changing the adipokine release by human adipose tissue, regardless of its origin. These effects are stronger in patients with mixed dyslipidemia and are particularly pronounced if atorvastatin and fenofibric acid are given together.
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PMID:Effect of atorvastatin and fenofibric acid on adipokine release from visceral and subcutaneous adipose tissue of patients with mixed dyslipidemia and normolipidemic subjects. 2008 Dec 49


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