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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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de Lima-Junior, Jose Carlos [1] ; Virginio, Vitor W. M. [1] ; Moura, Filipe A. [1, 2] ; Bertolami, Adriana [3] ; Bertolami, Marcelo [3] ; Coelho-Filho, Otavio R. [4] ; Zanotti, Ilaria [5] ; Nadruz, Wilson [4] ; de Faria, Eliana Cotta [6] ; de Carvalho, Luiz Sergio F. [4, 1] ; Sposito, Andrei C. [4, 1]
Total Authors: 11
Affiliation:
[1] Univ Estadual Campinas, Fac Med Sci, Lab Atherosclerosis & Vasc Biol, Sao Paulo - Brazil
[2] Brigham & Womens Hosp, Dept Cardiol, 75 Francis St, Boston, MA 02115 - USA
[3] Dante Pazzanese Cardiol Inst, Dept Dyslipidemia, Sao Paulo - Brazil
[4] Univ Estadual Campinas, Fac Med Sci, Dept Internal Med, Cardiol Div, Sao Paulo - Brazil
[5] Univ Parma, Dept Food & Drug, Parma - Italy
[6] Univ Estadual Campinas, Fac Med Sci, Dept Clin Pathol, Lipids Lab, Sao Paulo - Brazil
Total Affiliations: 6
Document type: Journal article
Source: NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES; v. 30, n. 2, p. 254-264, FEB 10 2020.
Web of Science Citations: 0
Abstract

Background and Aim: 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. Methods and Results: 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 beta = -0.054; CI 95% -0.0815, -0.0301). CEC, HDL-C, HDL size and HDLantioxidant activity were negatively associated with cIMT. BMI was inversely correlated with HDL-mediated inhibition of platelet aggregation (Spearman's rho -0.157, p < 0.03) and CEC (Spearman's rho -0.32, p < 0.001), but surprisingly it was directly correlated with the antioxidant activity (Spearman's rho 0.194, p = 0.052). Thus, even in non-obese, non-diabetic individuals, increased BMI is associated with a wide change in protective functions of HDL, reducing CEC and increasing antioxidant activity. In these subjects, decreased HDL concentration, size or function are related to increased atherosclerotic burden. Conclusion: Our findings demonstrate that in non-obese, non-diabetic individuals, the increasing values of BMI are associated with impaired protective functions of HDL and concomitant increase in atherosclerotic burden. (C) 2019 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved. (AU)

FAPESP's process: 10/00201-8 - Relationship between inflammatory markers and insulin resistance with subclinical atherosclerosis in patients with impaired fasting glucose
Grantee:Marcelo Chiara Bertolami
Support type: Regular Research Grants
FAPESP's process: 06/60585-9 - Relation of the plasma HDL-cholesterol concentration with blood monocyte and whole body cholesterol metabolism parameters
Grantee:Eder Carlos Rocha Quintão
Support type: Research Projects - Thematic Grants
FAPESP's process: 12/01645-2 - Additive role of qualitative characteristics of High-Density Lipoprotein (HDL) to its plasma quantification by cholesterol levels
Grantee:Natália Baratella Panzoldo
Support type: Scholarships in Brazil - Doctorate (Direct)