Gesundheitswesen 2017; 79(08/09): 656-804
DOI: 10.1055/s-0037-1605864
Vorträge
Georg Thieme Verlag KG Stuttgart · New York

HDL subspecies according to apoC-III and non-alcoholic fatty liver disease: The Multi-Ethnic Study of Atherosclerosis

M Koch
1   Harvard T.H. Chan School of Public Health, Nutrition Department, Boston
,
S Aroner
1   Harvard T.H. Chan School of Public Health, Nutrition Department, Boston
,
K Mukamal
1   Harvard T.H. Chan School of Public Health, Nutrition Department, Boston
2   Beth Israel Deaconess Medical Center, Department of Medicine, Boston
,
M Budoff
3   Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute, Los Angeles
,
R McClelland
4   University of Washington, School of Public Health, Seattle
,
M Jensen
1   Harvard T.H. Chan School of Public Health, Nutrition Department, Boston
5   Brigham and Women's Hospital, Channing Division of Network Medicine, Boston
› Author Affiliations
Further Information

Publication History

Publication Date:
01 September 2017 (online)

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Introduction:

Previously, we demonstrated that HDL is only inversely associated with cardiovascular disease and diabetes when it lacks the pro-inflammatory protein apolipoprotein C-III (apoC-III). To provide further insight into the cardiometabolic properties of HDL subspecies defined by the presence or absence of apoC-III, we examined these subspecies in relation to non-alcoholic fatty liver disease (NAFLD), a highly prevalent condition closely associated with the metabolic syndrome.

Methods:

We investigated cross-sectional associations between baseline (2000 – 2002) plasma levels of apoC-III-based HDL subspecies measured via ELISA and computed tomography-determined liver fat content (hepatic attenuation in Hounsfield units [HU]) among 5,009 participants in the Multi-Ethnic Study of Atherosclerosis without heavy alcohol consumption (> 14 drinks/week in men and > 7 drinks/week in women). Associations of HDL subspecies with continuous liver fat content and NAFLD (< 51 HU) were assessed using linear or logistic regression models, respectively, with adjustment for age, sex, race/ethnicity, study site, non-visceral adiposity, alcohol intake, smoking, and income.

Results:

Participants with higher levels of HDL without apoC-III had lower liver fat content (0.8 higher HU [95% CI: 0.4, 1.1 HU] per SD; p-linear < 0.0001). In contrast, no association was observed for HDL with apoC-III (0.1 higher HU [95% CI: -0.3, 0.5 HU] per SD; p-linear = 0.54; p-heterogeneity, HDL with and without apoC-III = 0.008). HDL with and without apoC-III were also differentially associated with NAFLD (HDL without apoC-III: OR per SD = 0.80; 95% CI: 0.72, 0.89 and HDL with apoC-III: OR per SD = 0.94; 95% CI: 0.85, 1.05; p-heterogeneity = 0.09).

Conclusion:

ApoC-III diminishes the inverse association between HDL and liver fat, supporting the existence of distinct apoC-III-defined HDL subspecies with respect to cardiometabolic disease risk.