| Hypercholesterolemia, a major risk factor for heart disease andstroke, is a complex disorder associated with genetic and environmental factors. Changes in human plasma cholesterol levels result from many environmental factors (e.g., dietary intake, exercise, smoking and genetic factors). Liver, as the regulation center of exogenous and endogenous lipids metabolism pathways, plays a especially important role in the balance of lipids metabolism. The effect of high-cholesterol and high-fat diet to the liver protein expression profile is seldom reported so far. We employ the technology of proteomics to compare the liver protein profiles of hypercholesterolemic and normal mice .The hypercholesterolemic mice were obtained after feeding atherogenic diet for 14 weeks. Protein extractions from mice liver were separated by two-dimensional electrophoresis and the gels were analysed with image analysis software. The differentially expressedproteins were identified primarily by mass spectrometry and then confirmed by comparing with the nice gel image in protein database Swiss Prot . The hypercholesterolemic mouse model has been successfully prepared. The protein extractions separated by two-dimensional electrophoresis have got high resolution and reproducibility. Sixteen differentially expressed protein spots (> 2 fold) have been found and 8 of which were identified as major urinary proteins(MUPs), carbonic anhydrase III and Glutathione S-transferase P2 . The under-expression of MUPs, carbonic anhydrase III and Glutathione S-transferase P2, which regulated by androgens, may be related to diet-induced hypercholesterolemia. Then we assayed the testosterone levels in the serum, liver and testis of hyperlipidemia mice and found that testosterone level in liver were lower than normal mice.The analysis of the changes of expression protein profile can help us to investigate the molecular marker of hypercholesterolemia and lays the basis for subsequent studies with atherosclerosis.
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