RESEARCH Open Access Unavailability of liver triac g H

For decades, high serum total cholesterol has been iden-tified as a clinical risk factor for atherosclerosis and car-diovascular disease [1,2]. The factors that determine serum total cholesterol levels are cholesterol synthesis in the body, which is controlled by genetic expression [3,4], and daily dietary intake [5,6]. Gene mutations related to cholesterol metabolism have been detected mainly in the region involved in serum lipoprotein metabolism [7]. As compositive matters of these factors, hyperresponders to dietary cholesterol, in whom serum cholesterol levels in-crease more than those of normal subjects after a high-cholesterol-diet period, have been reported by Katan et al. [8]. However, the causes and mechanisms for regu-lating sensitivity to dietary cholesterol remain unclear. Exogenously hypercholesterolemic (ExHC) rats were estab-lished from Sprague–Dawley (SD) rats as models for diet-induced hypercholesterolemia [9]. Their serum total cholesterol levels are increased only when fed a choles-terol diet. ExHC rats do not develop aortic atherosclerosis despite attempts to establish a model rat for atheroscler-osis [9]. Clarification of responsible genes and pathogenic mechanisms in ExHC rats will contribute to understandin