Cholic acid induces a Cftr dependent biliary secretion and liver growth response in mice.

The cause of Cystic fibrosis liver disease (CFLD), is unknown. It is well recognized that hepatic exposure to hydrophobic bile salts is associated with the development of liver disease. For this reason, we hypothesize that, CFTR dependent variations, in the hepatic handling of hydrophobic bile salts, are related to the development CFLD.

Postnatal treatment with dexamethasone perturbs hepatic and cardiac energy metabolism and is associated with a sustained atherogenic plasma lipid profile in suckling rats.

Early exposure to glucocorticoids (GC) has been proposed to disturb hepatic and cardiac function in later life. In the present study, we evaluated early metabolic alterations upon GC treatment that may predispose to long-term abnormalities. Rats were injected with dexamethasone (DEX) at d 1, 2, and 3 after birth and controls received saline (SAL).

Differential effects of streptozotocin-induced diabetes on expression of hepatic ABC-transporters in rats.

Background & Aims: Diabetes mellitus is associated with changes in bile formation. The aim of our study was to investigate the molecular basis for these changes in rats with experimentally induced diabetes.

Methods: Expression of bile canalicular transporters was studied by reverse-transcription polymerase chain reaction, immunoblotting, and immunohistochemistry in control, streptozotocin-diabetic, and insulin-treated diabetic rats.

Mdr P-glycoproteins are not essential for biliary excretion of the hydrophobic heme precursor protoporphyrin in a griseofulvin-induced mouse model of erythropoietic protoporphyria.

Hepatic complications in erythropoietic protoporphyria (EPP) have been attributed to toxic actions of accumulated protoporphyrin (PP). PP can only be removed via the bile but transport systems involved have not been defined. The aim of this study was to gain insight in the mode of biliary PP excretion, with emphasis on the potential contribution of the Mdr1 P-glycoprotein export pump and biliary lipids as PP carriers.