Fig. 5.

Hepatocyte-specific Cd36 deletion does not protect against LD-induced gallstone formation. Cd36-LKO mice were generated as described (Materials and Methods). A: DNA was extracted from hepatocytes (H) and the remnant, nonhepatocyte fraction of cells (O) after liver perfusion, and the DNA was analyzed by agarose gel. The hepatocyte fraction from Cd36- LKO mice shows Cre-mediated recombination. B: Hepatocytes were prepared from chow-fed Cd36-LKO mice and flox/flox controls, and extracts were subjected to Western blotting for CD36. C: Whole liver extracts were prepared from Cd36-LKO mice and flox/flox controls fed LD for 4 weeks and Western-blotted for CD36. D: Visible gallstones were observed in both Cd36-LKO and littermate control gallbladders (representative gross appearances of gallbladder in upper). Polarizing microscopy revealed aggregated ChMCs in both genotypes (lower; 200×). Gallstone incidence (E), gallstone score (F), and gallbladder volume (G) were determined as described in Materials and Methods. H: Hepatic lipids were extracted and quantitated enzymatically (Materials and Methods). Hepatic lipid content is expressed as μg/mg protein except FFA, which is expressed as nmol/mg protein. The data in C–E represent the mean ± SE. n = 4–6 per group. BA, bile acid, FC, free cholesterol; PL, phospholipid; TC, total cholesterol.