Excess weight mediates changes in HDL pool that reduce cholesterol efflux capacity and increase antioxidant activity

Obesity-related decline in high-density lipoprotein (HDL) functions such as cholesterol efflux capacity (CEC) has supported the notion that this lipoprotein dysfunction may contribute for atherogenesis among obese patients. We investigated if potentially other HDL protective actions may be affected...

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Veröffentlicht in:Nutrition, metabolism, and cardiovascular diseases metabolism, and cardiovascular diseases, 2020-02, Vol.30 (2), p.254-264
Hauptverfasser: de Lima-Junior, Jose Carlos, Virginio, Vitor W.M., Moura, Filipe A., Bertolami, Adriana, Bertolami, Marcelo, Coelho-Filho, Otavio R., Zanotti, Ilaria, Nadruz, Wilson, de Faria, Eliana Cotta, de Carvalho, Luiz Sergio F., Sposito, Andrei C.
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Sprache:eng
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Zusammenfassung:Obesity-related decline in high-density lipoprotein (HDL) functions such as cholesterol efflux capacity (CEC) has supported the notion that this lipoprotein dysfunction may contribute for atherogenesis among obese patients. We investigated if potentially other HDL protective actions may be affected with weight gain and these changes may occur even before the obesity range in a cross-sectional analysis. Lipid profile, body mass index (BMI), biochemical measurements, and carotid intima-media thickness (cIMT) were obtained in this cross-sectional study with 899 asymptomatic individuals. Lipoproteins were separated by ultracentrifugation and HDL physical-chemical characterization, CEC, antioxidant activity, anti-inflammatory activity, HDL-mediated platelet aggregation inhibition were measured in a randomly-selected subgroup (n = 101). Individuals with increased HDL-C had an attenuated increase in cIMT with elevation of BMI (interaction effect β = −0.054; CI 95% −0.0815, −0.0301). CEC, HDL-C, HDL size and HDL-antioxidant activity were negatively associated with cIMT. BMI was inversely correlated with HDL-mediated inhibition of platelet aggregation (Spearman's rho −0.157, p 
ISSN:0939-4753
1590-3729
DOI:10.1016/j.numecd.2019.09.017