Gallbladder motility and gut hormone plasma levels in subjects with and without gallstones.

Hormonal control of gallbladder motility is still unclear in patients with cholelithiasis. In a case-control study, we determined the characteristics of gallbladder emptying evaluated sonographically and the hormone levels of somatostatin, gastrin, and pancreatic polypeptide, before and after a fatty meal in 10 gallstone patients compared with 20 healthy subjects. Patients with lithiasis had a larger residual volume (median 12,0 ml vs 6,5 ml; P = 0.

Conjugation with taurine prevents side-chain desaturation of ursodeoxycholic and beta-muricholic acids in bile fistula rats.

The metabolism of intravenously infused bile salts, tauroursodeoxycholate, tauro-beta-muricholate and their corresponding unconjugated forms in the liver was investigated in bile salt-depleted bile fistula rats. The biliary bile salt composition was determined by gas chromatography-mass spectrometry using chemical positive ionization and electron-impact methods. For an infusion rate of 2 micromol/min/kg, all bile salts were efficiently secreted in bile, inducing similar choleresis.

Bile salts modulate chronic ethanol-induced hepatotoxicity.

This study tested the hypothesis that chronic ethanol-induced injury in rats may be modified by the hydrophobicity of the bile acid pool. The supplementation to chronic ethanol feeding (28 days) with chenodeoxycholate, a hydrophobic bile salt, aggravated steatosis (accumulation of triacylglycerols and cholesterol esters), lipoperoxidation and cytolysis (expressed as elevations of activities of aspartate aminotransferase and glutamate dehydrogenase), while the addition of ursodeoxycholic acid, a hydrophilic bile salt, alleviated ethanol-induced hepatic alterations. Furthermore, our data show that ursodeoxycholic acid still exerts its beneficial effects in a model of more severe hepatic intoxication induced by the co-administration of ethanol and chenodeoxycholic acid.

[Ursodeoxycholic acid and prevention of tacrine-induced hepatotoxicity: a pilot study].

Ursodeoxycholic acid is a protective agent against liver toxicity caused by some drugs. In the present pilot study, we assessed the effect of this bile acid on tacrine-induced hepatotoxicity. Fourteen patients with a diagnosis of Alzheimer's disease received tacrine and ursodeoxycholic acid (13 mg/kg/day) for 105 days.