Effect of a high-fat–high-cholesterol diet on gallbladder bile acid composition and gallbladder motility in dogs

Abstract

OBJCTIVE To investigate the effects of dietary lipid overload on bile acid metabolism and gallbladder motility in healthy dogs. ANIMALS 7 healthy Beagles. PROCEDURES In a crossover study, dogs were fed a high-fat-high-cholesterol diet (HFCD) or a low-fat diet (LFD) for a period of 2 weeks. After a 4-month washout period, dogs were fed the other diet for 2 weeks. Before and at the end of each feeding period, the concentrations of each of the gallbladder bile acids, cholecystokinin (CCK)-induced gallbladder motility, and bile acid metabolism-related hepatic gene expression were examined in all dogs. RESULTS The HFCD significantly increased plasma total cholesterol concentrations. The HFCD also increased the concentration of taurochenodeoxycholic acid and decreased the concentration of taurocholic acid in bile and reduced gallbladder contractility, whereas the LFD significantly decreased the concentration of taurodeoxycholic acid in bile. Gene expression analysis revealed significant elevation of cholesterol 7α-hydroxylase mRNA expression after feeding the HFCD for 2 weeks, but the expression of other genes was unchanged. CONCLUSIONS AND CLINICAL RELEVANCE Feeding the HFCD and LFD for 2 weeks induced changes in gallbladder bile acid composition and gallbladder motility in dogs. In particular, feeding the HFCD caused an increase in plasma total cholesterol concentration, an increase of hydrophobic bile acid concentration in bile, and a decrease in gallbladder sensitivity to CCK. These results suggested that similar bile acid compositional changes and gallbladder hypomotility might be evident in dogs with hyperlipidemia.

Risk Factors for Cholesterol Polyp Formation In The Gallbladder - Closely Related to Lipid Metabolism

“…High LDL can promote the formation of cholesterol polyps by lowering the sensitivity of gallbladder to cholecystokinin, which subsequent decreased gallbladder contraction, cholestasis and relative de ciency of cholic acid. [15][16][17] These physiological changes could promote cholesterol crystallization and polyp formation. While, Wu et al [8] found that TG, TC, HDL, and LDL showed no statistical differences between the cholesterol polyp group and the non-cholesterol polyp group, indicating that lipid levels may only play a partial role in the formation of cholesterol polyps.…”

Risk factors for cholesterol polyp formation in the gallbladder are closely related to lipid metabolism

“…LDL is representative of the status of liver anabolism and cholesterol transport. High LDL can promote the formation of cholesterol polyps by lowering the sensitivity of the gallbladder to cholecystokinin, which subsequently results in decreased gallbladder contraction, cholestasis, and a relative deficiency of cholic acid [15][16][17]. Meanwhile, the formation of cholesterol polyps may be related to abnormal reverse cholesterol transport related to HDL.…”

Bile cholesterol and viscosity, the keys to discriminating adenomatous polyps from cholesterol polyps by a novel predictive scoring model

“…If there is abnormal bile secretion or functional impairment of the gallbladder, the bile contents stored in the gallbladder will change accordingly [ 12 ]. Several studies [ 13 , 14 ] have reported that dyslipidemia, such as high low-density lipoprotein, would decrease gallbladder sensitivity to cholecystokinin and inhibit cholecystokinin secretion, resulting in a reduction of gallbladder motility and alteration of the mucosal esterification of free sterols from bile. This physiological change in the hepatic cholesterol mechanism could then promote cholesterol polyp formation.…”