Differences between hepatic and biliary lipid metabolism and secretion in genetically gallstone-susceptible and gallstone-resistant mice.

Nov 2, 2002Chinese medical journal

Differences in liver and bile fat processing and release in mice prone or resistant to gallstones

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Circadian Biology on OpenScience ↗PubMed ↗

Abstract

Hepatic secretion rates of biliary lipids in C57L mice were significantly higher than in AKR mice both before and after a lithogenic diet.

C57L mice exhibited markedly higher secretion rates of all biliary lipids compared to AKR mice (P < 0.05, P < 0.01).
Hepatic cholesterol content was significantly lower in C57L mice than in AKR mice (P < 0.05).
After the lithogenic diet, C57L mice showed a significantly greater increase in biliary cholesterol secretion compared to AKR mice (P < 0.01).
Cholesterol gallstones formed in C57L mice, while AKR mice developed fatty livers.
Biliary cholesterol hypersecretion may be a key factor in the susceptibility to gallstone formation in C57L mice.

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OBJECTIVE: To investigate differences between hepatic and biliary lipid metabolism and secretion of genetically gallstone-susceptible (C57L) and resistant (AKR) mice and the mechanism of cholesterol gallstone formation.

METHODS: The inbred C57L and AKR mice were fed a lithogenic diet containing 15% fat, 1.25% cholesterol and 0.5% cholic acid for four weeks. Hepatic cholesterol content and secretion rates of biliary lipids, as well as phenotypes of the liver and gallbladder were determined and examined before and after the feeding of the lithogenic diet.

RESULTS: Both before and after ingestion of the lithogenic diet, hepatic secretion rates of all biliary lipids in C57L mice were markedly higher than that of AKR mice (P < 0.05, P < 0.01, respectively), whereas hepatic cholesterol contents of C57L mice were significantly lower than that of AKR mice (P < 0.05). Furthermore, after consumption of the lithogenic diet, the increase in hepatic secretion rate of biliary cholesterol in C57L mice was significantly higher than that in AKR mice (P < 0.01). Cholesterol gallstones formed in C57L mice and fatty livers developed in AKR mice.

CONCLUSIONS: Biliary cholesterol hypersecretion is the key pathophysiological defect of gallstone formation, lith genes have effects on biliary cholesterol hypersecretion and susceptibility to cholesterol gallstone formation in C57L mice. Lithogenic bile is formed at the canalicular membrane and precedes the development of cholesterol gallstones. It is most likely that cholesterol and bile acid hyposecretion make the AKR strain susceptible to the development of fatty livers and resistant to gallstone formation.

Differences between hepatic and biliary lipid metabolism and secretion in genetically gallstone-susceptible and gallstone-resistant mice.

Abstract

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