Ginger Resistant Starch Regulates Lipids and Bile Acid Metabolism in Hyperlipidemic Rats

In order to study the hypolipidemic effect of different types of ginger resistant starch on experimentally induced hyperlipidemia in rats, physiological and biochemical indicators of hyperlipidemic rats were measured, and histopathological characteristics of blood vessel, colon and liver tissues were examined. By measuring the contents of primary and secondary bile acids in serum, a serum metabolic profile of bile acids was constructed. The results showed that compared to the hyperlipidemic model (HM) group, the body mass and liver index of rats in the positive control (PC, simvastatin), ginger resistant starch type 2 (GRS2), ginger resistant starch type 3 (GRS3), ginger resistant starch type 4 (GRS4) and high amylose maize starch (HMS) groups were significantly reduced, PC and GRS4 being the most effective in this regard. Simvastatin, ginger resistant starch and HMS significantly reduced the contents of total triglyeride (TG), total cholesterol (TCHO), low density lipoprotein cholesterol (LDL-C), and the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (P < 0.05), and increased the level of high density lipoprotein cholesterol (HDL-C) in the rat serum (P < 0.05), and the best effect was found with GRS3 and GRS4. According to histopathological observation, ginger resistant starch could improve the vascular layer, intimal structure and outer wall structure of hyperlipidemia rats, increase the thickness of the colonic muscularis, the thickness of the mucous membrane and the length of villi, make the structure of colonic crypts and goblet cells clearer, and reduce the number and size of fat vacuoles in the liver cytoplasm. In this regard, GRS3 and GRS4 were more effective than HMS. In addition, GRS3 and GRS4 improved lipid metabolism in hyperlipidemic rats mainly by reducing the contents of free primary bile acids (cholic acid, chenodeoxycholic acid, β-murocholic acid and α-murocholic acid) and deoxygenated secondary bile acids (hyodeoxycholic acid, ursodeoxycholic acid, deoxycholic acid, taurohyodeoxycholic acid and glycoursodeoxycholic acid) in the serum.