The role of transhepatic bile salt flux in the control of hepatic secretion of triacylglycerol-rich lipoproteins in vivo in rodents.

Bile salts (BS) have been shown to suppress the secretion of very-low-density lipoprotein-triglyceride (VLDL-TG) in rat and human hepatocytes in vitro. In the present study, we investigated whether the transhepatic BS flux affects VLDL-TG concentration and hepatic VLDL-TG secretion in vivo. In rats, the transhepatic BS flux was quantitatively manipulated by 1-week chronic bile diversion (BD), followed by intraduodenal infusion with taurocholate (TC) or saline for 6 h.

Fat malabsorption in essential fatty acid-deficient mice is not due to impaired bile formation.

Essential fatty acid (EFA) deficiency induces fat malabsorption, but the pathophysiological mechanism is unknown. Bile salts (BS) and EFA-rich biliary phospholipids affect dietary fat solubilization and chylomicron formation, respectively. We investigated whether altered biliary BS and/or phospholipid secretion mediate EFA deficiency-induced fat malabsorption in mice.

Stimulation of lipogenesis by pharmacological activation of the liver X receptor leads to production of large, triglyceride-rich very low density lipoprotein particles.

The oxysterol-activated liver X receptor (LXR) provides a link between sterol and fatty acid metabolism; activation of LXR induces transcription of lipogenic genes. This study shows that induction of the lipogenic genes Srebp-1c, Fas, and Acc1 upon administration of the synthetic LXR agonist T0901317 to C57BL/6J mice (10 mg/kg/day, 4 days) is associated with massive hepatic steatosis along the entire liver lobule and a 2.5-fold increase in very low density lipoprotein-triglyceride (VLDL-TG) secretion.

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.

Functional development of fat absorption in term and preterm neonates strongly correlates with ability to absorb long-chain Fatty acids from intestinal lumen.

Our goal for this study was to determine whether the maturation of fat absorption in neonatal life is functionally related to an increased ability to hydrolyze dietary fat, to absorb long-chain fatty acids, or to do both. In 16 preterm and in eight term neonates, the intestinal ability to hydrolyze triacylglycerols and the capacity to absorb long-chain fatty acids were determined at several times between birth and 5 mo after the term age. These processes were compared with the percentage of fat absorption (formula-fed infants) or with fecal fat excretion (breast-fed infants).