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Van Wijk J.P.H.,University Utrecht | Cabezas M.C.,Center for Diabetes and Vascular Medicine
International Journal of Vascular Medicine | Year: 2012

The use of combination antiretroviral therapy (CART) in HIV-infected patients has resulted in a dramatic decline in AIDS-related mortality. However, mortality due to non-AIDS conditions, particularly cardiovascular disease (CVD) seems to increase in this population. CART has been associated with several metabolic risk factors, including insulin resistance, low HDL-cholesterol, hypertriglyceridemia and postprandial hyperlipidemia. In addition, HIV itself, as well as specific antiretroviral agents, may further increase cardiovascular risk by interfering with endothelial function. As the HIV population is aging, CVD may become an increasingly growing health problem in the future. Therefore, early diagnosis and treatment of cardiovascular risk factors is warranted in this population. This paper reviews the contribution of both, HIV infection and CART, to insulin resistance, postprandial hyperlipidemia and cardiovascular risk in HIV-infected patients. Strategies to reduce cardiovascular risk are also discussed. © 2012 Jeroen P. H. van Wijk and Manuel Castro Cabezas.

Van Wijk J.P.H.,University Utrecht | Hoepelman A.I.M.,University Utrecht | De Koning E.J.P.,Leiden University | Rabelink T.J.,Leiden University | Cabezas M.C.,Center for Diabetes and Vascular Medicine
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2011

Objective- To compare the effects of rosiglitazone (8 mg/d, n=19) and metformin (2 g/d, n=18) on postprandial lipemia in patients with HIV-lipodystrophy. Methods and results- Lipodystrophy in HIV is associated with insulin resistance and disturbed postprandial triglyceride and free fatty acid (FFA) metabolism. We conducted an open randomized 6-month study with standardized 10-h oral fat-loading tests at baseline and after treatment. Rosiglitazone (-34%) and metformin (-37%) reduced homeostasis model assessment similarly (P<0.05). Rosiglitazone did not change the area under the curve for FFA and triglyceride; however, it did reduce the area under the curve for hydroxybutyric acid (a marker of hepatic FFA oxidation) by 25% (P<0.05). Rosiglitazone increased the area under the curve for remnantlike particle cholesterol by 40% (P<0.01) compared with baseline. Metformin did not change any of the postprandial measurements. Conclusion- Rosiglitazone improved insulin sensitivity and decreased postprandial hydroxybutyric acid levels in patients with HIV-lipodystrophy, suggesting improved FFA handling. Despite metabolic improvements, rosiglitazone caused a marked increase in postprandial remnantlike particle cholesterol, which may adversely affect cardiovascular risk. Metformin did not affect postprandial lipemia and could be used to treat insulin resistance in this population. © 2011 American Heart Association. All rights reserved.

Klop B.,Center for Diabetes and Vascular Medicine | Castro Cabezas M.,Center for Diabetes and Vascular Medicine
Current Cardiovascular Risk Reports | Year: 2012

Cardiovascular disease can be considered a condition of chronic low-grade inflammation. Postprandial hyperlipidemia and obesity can both exacerbate inflammatory processes. Postprandial lipemia stimulates the activation of leukocytes, the production of chemokines, and activation of the complement system. Obesity is also associated with postprandial hyperlipidemia by hepatic overproduction of very low-density lipoprotein (VLDL) and consequently delayed clearance of intestinally derived chylomicrons due to competition for the same metabolic pathways. Insulin resistance is one of the key elements leading to hepatic VLDL overproduction and is also a key factor in the generation of inflammation. These metabolic derangements cause accumulation of atherogenic remnant lipoproteins, which is also a proatherogenic mechanism. Change in lifestyle is the most important therapeutic strategy to stop this vicious circle of postprandial hyperlipidemia, obesity, inflammation, insulin resistance, and cardiovascular disease. © 2011 Springer Science+Business Media, LLC.

Klop B.,Center for Diabetes and Vascular Medicine | Proctor S.D.,University of Alberta | Mamo J.C.,Curtin University Australia | Botham K.M.,Royal Veterinary College | Castro Cabezas M.,Center for Diabetes and Vascular Medicine
International Journal of Vascular Medicine | Year: 2012

Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. Remnant lipoproteins become attached to the vascular wall, where they can penetrate intact endothelium causing foam cell formation. Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate the expression of endothelial adhesion molecules, facilitate adhesion and migration of inflammatory cells into the subendothelial space, and activate the complement system. Since humans are postprandial most of the day, the continuous generation of remnants after each meal may be one of the triggers for the development of atherosclerosis. Modulation of postprandial lipemia by lifestyle changes and pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options. © 2012 Boudewijn Klop et al.

Klop B.,Center for Diabetes and Vascular Medicine | Rego A.T.D.,Institute for Health Research | Cabezas M.C.,Center for Diabetes and Vascular Medicine
Current Opinion in Lipidology | Year: 2013

Purpose of review: This study reviews recent developments concerning the effects of alcohol on plasma triglycerides. The focus will be on population, intervention and metabolic studies with respect to alcohol and plasma triglycerides. Recent findings: Alcohol consumption and fat ingestion are closely associated and stimulated by each other via hypothalamic signals and by an elevated cephalic response. A J-shaped relationship between alcohol intake and plasma triglycerides has been described. A normal body weight, polyphenols in red wine and specific polymorphisms of the apolipoprotein A-V and apolipoprotein C-III genes may protect against alcohol-associated hypertriglyceridemia. In contrast, obesity exaggerates alcohol-associated hypertriglyceridemia and therefore the risk of pancreatitis. Summary: High alcohol intake remains harmful since it is associated with elevated plasma triglycerides, but also with cardiovascular disease, alcoholic fatty liver disease and the development of pancreatitis. Alcohol-induced hypertriglyceridemia is due to increased very-low-density lipoprotein secretion, impaired lipolysis and increased free fatty acid fluxes from adipose tissue to the liver. However, light to moderate alcohol consumption may be associated with decreased plasma triglycerides, probably determined by the type of alcoholic beverage consumed, genetic polymorphisms and lifestyle factors. Nevertheless, patients should be advised to reduce or stop alcohol consumption in case of hypertriglyceridemia. © 2013 Wolters Kluwer Health.

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