Table 1.
Clinical, serological and histological characteristics of the primary and validation cohorts.
Table 2.
Serum lipid levels and lipoprotein subclasses in the primary and validation cohorts.
Figure 1.
Relationship between LDL-MI, as determined by PAGE, and sdLDL concentrations, measured by HPLC, in 49 patients with NAFLD.
LDL-MI was significantly correlated with sdLDL concentrations (r = 0.843, P<0.001).
Table 3.
Clinical characteristics of patients with NAFLD and low or high LDL-MI.
Table 4.
Multiple regression analysis of factors associated with increased LDL-MI in patients with NAFLD.
Figure 2.
Effects of the lipid lowering drugs (A) ezetimibe, (B) fibrate, and (C) atorvastatin on LDL-MI in patients with NAFLD.
All data are expressed as the mean ± SD. Statistical significance was determined using Student's t-test.
Figure 3.
LDL-MI in patients with various liver diseases including NAFLD.
LDL-MI was significantly higher in patients with NAFLD patients than in patients with with ALD, CH-C, CH-B, AIH and PBC. Shown are the interquartile ranges (boxes), medians (dots), and ranges (vertical lines).
Figure 4.
Mechanisms of increased LDL-MI, an indicator of sdLDL, in patients with NASH.
Microsomal triglyceride transfer protein activity is much lower in the livers of patients with NASH than with NAFL, resulting in decreased synthesis of total VLDL and increased synthesis of TG-rich VLDL (VLDL1) [13], leading to an increase in sdLDL [16]. The incidence of atherosclerotic diseases may therefore be quite high in patients with NASH.