Dyslipidemia in the metabolic syndrome and type 2 diabetes mellitus

Brunzell, John D.; Ayyobi, Amir F

doi:10.1016/j.amjmed.2003.08.011

Cited by 134 publications

(93 citation statements)

References 49 publications

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“…Accordingly, a genetic study shows that overexpression of p22 phox increases the NADPH oxidase activity in mice aortas (38). The clinical relevance of these findings is underlined by a recent study showing that thiazolidinediones, which can beneficially influence insulin resistance (39), reduce the expression of the NADPH oxidase p22 phox subunit (40). In the present study, we show for the first time that metabolic syndrome patients exhibit enhanced levels of nitrotyrosine.…”

Section: Discussionsupporting

confidence: 54%

Phagocytic NADPH Oxidase Overactivity Underlies Oxidative Stress in Metabolic Syndrome

et al. 2006

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Oxidative stress plays a critical role in the pathogenesis of atherosclerosis in patients with metabolic syndrome. This study aimed to investigate whether a relationship exists between phagocytic NADPH oxidase activity and oxidative stress and atherosclerosis in metabolic syndrome patients. The study was performed in 56 metabolic syndrome patients (metabolic syndrome group), 99 patients with one or two cardiovascular risk factors (cardiovascular risk factor group), and 28 healthy subjects (control group). NADPH oxidase expression and activity was augmented (P < 0.05) in metabolic syndrome compared with cardiovascular risk factor and control groups. Insulin was enhanced (P < 0.05) in metabolic syndrome patients compared with cardiovascular risk factor and control groups and correlated with NADPH oxidase activity in the overall population. Insulin stimulated NADPH oxidase activity; this effect was abolished by a specific protein kinase C inhibitor. Oxidized LDL and nitrotyrosine levels and carotid intima-media thickness were increased (P < 0.05) in the metabolic syndrome group compared with cardiovascular risk factor and control groups and correlated with NADPH oxidase activity in the overall population. These findings suggest that phagocytic NADPH oxidase overactivity is involved in oxidative stress and atherosclerosis in metabolic syndrome patients. Our findings also suggest that hyperinsulinemia may contribute to oxidative stress in metabolic syndrome patients through activation of NADPH oxidase. Diabetes 55: 209 -215, 2006

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Section: Discussionsupporting

confidence: 54%

Phagocytic NADPH Oxidase Overactivity Underlies Oxidative Stress in Metabolic Syndrome

et al. 2006

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“…Hypertriglyceridemia, as one of the components of the MS, is closely related to a constellation of metabolic risk factors including a central distribution of adiposity or visceral obesity, insulin resistance, impaired glucose tolerance, hypertension, and high TG and/or low HDL-C, associated with an atherogenic, procoagulant, and proinflammatory state [56][57][58][59][60][61][62][63][64].…”

Section: Hypertriglyceridemia As a Major Component Of Atherogenic Dysmentioning

confidence: 99%

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Tenenbaum

Klempfner

Fisman

2014

Cardiovasc Diabetol

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The existence of an independent association between elevated triglyceride (TG) levels, cardiovascular (CV) risk and mortality has been largely controversial. The main difficulty in isolating the effect of hypertriglyceridemia on CV risk is the fact that elevated triglyceride levels are commonly associated with concomitant changes in high density lipoprotein (HDL), low density lipoprotein (LDL) and other lipoproteins. As a result of this problem and in disregard of the real biological role of TG, its significance as a plausible therapeutic target was unfoundedly underestimated for many years. However, taking epidemiological data together, both moderate and severe hypertriglyceridaemia are associated with a substantially increased long term total mortality and CV risk. Plasma TG levels partially reflect the concentration of the triglyceride-carrying lipoproteins (TRL): very low density lipoprotein (VLDL), chylomicrons and their remnants. Furthermore, hypertriglyceridemia commonly leads to reduction in HDL and increase in atherogenic small dense LDL levels. TG may also stimulate atherogenesis by mechanisms, such excessive free fatty acids (FFA) release, production of proinflammatory cytokines, fibrinogen, coagulation factors and impairment of fibrinolysis. Genetic studies strongly support hypertriglyceridemia and high concentrations of TRL as causal risk factors for CV disease. The most common forms of hypertriglyceridemia are related to overweight and sedentary life style, which in turn lead to insulin resistance, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Intensive lifestyle therapy is the main initial treatment of hypertriglyceridemia. Statins are a cornerstone of the modern lipids-modifying therapy. If the primary goal is to lower TG levels, fibrates (bezafibrate and fenofibrate for monotherapy, and in combination with statin; gemfibrozil only for monotherapy) could be the preferable drugs. Also ezetimibe has mild positive effects in lowering TG. Initial experience with en ezetimibe/fibrates combination seems promising. The recently released IMPROVE-IT Trial is the first to prove that adding a non-statin drug (ezetimibe) to a statin lowers the risk of future CV events. In conclusion, the classical clinical paradigm of lipids-modifying treatment should be changed and high TG should be recognized as an important target for therapy in their own right. Hypertriglyceridemia should be treated.

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“…El TA constituye uno de los órganos clave en la homeostasis energética, el cual regula sus propias características funcionales y morfológicas de acuerdo con las condiciones fisiológicas o patológicas predominantes, incluida la homeostasis asociada al sobrepeso y la obesidad 1 . Como consecuencia adversa, la capacidad de almacenar grasa tiene con frecuencia un valor negativo, debido al consumo excesivo por la dieta 2 , con secuelas metabólicas y otros estados hiperlipidémicos 3 , entre los cuales se detectan una concentración elevada de Triglicéridos (TG) 4 , alteraciones del ciclo metabólico de los Ácidos Grasos Libres (AGL), colesterol total corporal y Lipoproteínas de Baja Densidad (LDL, Low Density Lipoprotein) y de Muy Baja Densidad (VLDL, Very Low Density Lipoprotein) en sangre.…”

Section: N T R O D U C C I ó Nunclassified

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

Barrientos‐Alvarado

Vázquez²,

Oscoy³

et al. 2014

Rev. Nutr.

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ObjetivoEste estudio evaluó el efecto de la glucosamina oral en el sobrepeso y dislipidemia provocada por una dieta hipercalórica en ratas. MétodosEn 4 grupos de ratas Wistar: alimentados con dieta comercial para roedores y agua de beber sin grupo de control y con glucosamina (500 mg/kg-1 por día) grupo glucosamina y con dieta hipercalórica enriquecida al 24% (g/g) compuesta por manteca de cerdo y agua de beber sin grupo hipercalórico y con glucosamina grupo hipercalórico + grupo glucosamina, durante 22 semanas, se evaluaron el peso corporal, grasa abdominal, niveles de glucemia, triglicéridos, colesterol total y lipoproteínas de alta densidad en suero. ResultadosSe observó un aumento del peso corporal y glucemia en suero con dislipidemias en el grupo con dieta hipercalórica grupo hipercalórico versus grupo de controle (p<0.001); al administrarse glucosamina para esta misma dieta grupo hipercalórico + grupo glucosamina se minimizaron los efectos presentados, disminuyendo la cantidad de grasa abdominal y los niveles del perfil lípido en suero (p>0.05) y regulándose el peso corporal, las lipoproteínas de alta densidad y la glucemia basal (p<0.05). ConclusionLa glucosamina reguló el peso corporal y la glucemia en sangre y minimizó las dislipidemias provocadas por la dieta hipercalórica, favoreciendo el aumento de colesterol lipoproteínas de alta densidad en las ratas. No afectó el peso corporal y el metabolismo lipídico cuando se administró con dieta comercial.Palabras ilave: Glucemia. Glucosamina. HDL-colesterol. Peso corporal. A B S T R A C T Objective This study evaluated the effect of oral glucosamine on overweight and dyslipidemia caused by a high-fat diet in rats. Methods Four groups of Wistar rats: fed with commercial rodent food and drinking water without (control group) and with glucosamine (500 mg kg-1 per day) and a high-fat diet enriched with 24% (g/g) butter pork and drinking water without and with glucosamine, for 22 weeks; the body weight, abdominal fat, blood glucose, triglycerides, total cholesterol, and high density lipoprotein in serum were evaluated. Results Body

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Dyslipidemia in the metabolic syndrome and type 2 diabetes mellitus

Cited by 134 publications

References 49 publications

Phagocytic NADPH Oxidase Overactivity Underlies Oxidative Stress in Metabolic Syndrome

Phagocytic NADPH Oxidase Overactivity Underlies Oxidative Stress in Metabolic Syndrome

Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

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