Eline H van den Berg1, Eke G Gruppen2, Sanam Ebtehaj3, Stephan J L Bakker4, Uwe J F Tietge3, Robin P F Dullaart5. 1. Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands; Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, The Netherlands. 2. Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands; Department of Nephrology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands. 3. Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands. 4. Department of Nephrology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713GZ, Groningen, The Netherlands. 5. Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands. Electronic address: R.P.F.Dullaart@umcg.nl.
Abstract
BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) parallels the obesity epidemic and associates with components of the metabolic syndrome (MetS). Cholesterol efflux capacity (CEC) represents a key metric of high density lipoprotein (HDL) function which may predict atherosclerotic cardiovascular disease (CVD). Here we assessed the relationship of CEC with NAFLD. METHODS: CEC was determined from THP-1 macrophage foam cells towards apolipoprotein B-depleted plasma among 639 subjects (454 men; 36 subjects with type 2 diabetes mellitus (T2D); 226 with MetS), participating in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study. A Fatty Liver Index (FLI) ≥ 60 was used as a proxy of NAFLD. RESULTS: 372 participants had a FLI ≥60, which coincided with an increased prevalence of T2D and MetS (p = 0.009 and p < 0.001), as well as with central obesity, higher systolic blood pressure, glucose, total cholesterol, triglycerides and high sensitivity C-reactive protein (hsCRP), and decreased HDL cholesterol (p < 0.001 for each). In multivariable linear regression analyses, CEC was inversely associated with an elevated FLI, when taking account of clinical covariates (fully adjusted model: β = -0.091, p = 0.043), and alternatively when taking account of systolic blood pressure, waist/hip ratio, glucose, HDL cholesterol, triglycerides and hsCRP (fully adjusted model: β = -0.103, p = 0.034). CONCLUSIONS: Impaired CEC is associated with NAFLD, as inferred from a FLI≥60, even when taking account of lower HDL cholesterol and enhanced low-grade chronic inflammation. Reduced CEC could contribute to accelerated CVD in NAFLD patients.
BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) parallels the obesity epidemic and associates with components of the metabolic syndrome (MetS). Cholesterol efflux capacity (CEC) represents a key metric of high density lipoprotein (HDL) function which may predict atherosclerotic cardiovascular disease (CVD). Here we assessed the relationship of CEC with NAFLD. METHODS: CEC was determined from THP-1 macrophage foam cells towards apolipoprotein B-depleted plasma among 639 subjects (454 men; 36 subjects with type 2 diabetes mellitus (T2D); 226 with MetS), participating in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study. A Fatty Liver Index (FLI) ≥ 60 was used as a proxy of NAFLD. RESULTS: 372 participants had a FLI ≥60, which coincided with an increased prevalence of T2D and MetS (p = 0.009 and p < 0.001), as well as with central obesity, higher systolic blood pressure, glucose, total cholesterol, triglycerides and high sensitivity C-reactive protein (hsCRP), and decreased HDL cholesterol (p < 0.001 for each). In multivariable linear regression analyses, CEC was inversely associated with an elevated FLI, when taking account of clinical covariates (fully adjusted model: β = -0.091, p = 0.043), and alternatively when taking account of systolic blood pressure, waist/hip ratio, glucose, HDL cholesterol, triglycerides and hsCRP (fully adjusted model: β = -0.103, p = 0.034). CONCLUSIONS: Impaired CEC is associated with NAFLD, as inferred from a FLI≥60, even when taking account of lower HDL cholesterol and enhanced low-grade chronic inflammation. Reduced CEC could contribute to accelerated CVD in NAFLD patients.
Authors: Negar Sarmadi; Hossein Poustchi; Fatemeh Ali Yari; Amir Reza Radmard; Sara Karami; Abbas Pakdel; Parisa Shabani; Ali Khaleghian Journal: PLoS One Date: 2022-04-12 Impact factor: 3.240
Authors: Bart J Verwer; Peter G Scheffer; Rick P Vermue; Petra J Pouwels; Michaela Diamant; Maarten E Tushuizen Journal: Liver Int Date: 2020-07-25 Impact factor: 5.828