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Intravenous ursodeoxycholic acid reduces cholestasis in parenterally fed newborn piglets
D R Duerksen1, J E Van Aerde, L Gramlich
1Department of Medicine, University of Alberta, Edmonton, Canada.
Insights
Intravenous ursodeoxycholic acid (UDCA) improved bile flow and reduced bilirubin in piglets with total parenteral nutrition (TPN)-induced cholestasis. UDCA did not normalize bile composition but enhanced hepatocyte function.
Area of Science:
- Neonatal physiology
- Gastroenterology
- Hepatology
Background:
- Cholestasis is a common complication of total parenteral nutrition (TPN) in preterm infants.
- Ursodeoxycholic acid (UDCA) is a potential therapeutic agent for cholestatic conditions.
Purpose of the Study:
- To investigate whether intravenous UDCA can prevent TPN-induced cholestasis in piglets.
- To assess UDCA's effects on bile flow, bile composition, and hepatocyte membrane function.
Main Methods:
- Piglet model with three groups: sow's milk, TPN, and TPN with intravenous UDCA.
- Measurement of basal and stimulated bile flow after 3 weeks.
- Analysis of bile and hepatocyte membrane composition, including lipids and Na+,K(+)-ATPase activity.
Main Results:
- TPN significantly reduced bile acid secretion and bile flow compared to controls.
- Intravenous UDCA treatment improved bile flow and hepatocyte Na+,K(+)-ATPase activity in TPN-fed piglets.
- UDCA did not normalize TPN-induced alterations in bile composition, but sinusoidal membrane fluidity was preserved.
Conclusions:
- Intravenous UDCA effectively improves bile flow and reduces bilirubin levels in TPN-induced cholestasis in piglets.
- UDCA demonstrates a protective effect on hepatocyte function, although bile composition normalization was not observed.
Background & Aims:
Cholestasis complicates total parenteral nutrition (TPN) in preterm infants. Ursodeoxycholic acid (UDCA) is used for several cholestatic problems. The hypothesis of this study was that intravenous UDCA prevents TPN-induced cholestasis by (1) maintaining normal basal and stimulated bile flow, (2) altering bile composition, and (3) changing hepatocyte membrane composition and Na+,K(+)-adenosine triphosphatase (ATPase) activity.
Methods:
Three groups of piglets were studied: group 1 received sow's milk, groups 2 and 3 received TPN, and group 3 also received 100 mumol.kg-1.day-1 UDCA intravenously. After 3 weeks, basal and stimulated bile flow were measured. Cholesterol, bile acids, phospholipids, and phospholipid fatty acids were analyzed in bile, and fluidity, phospholipid fatty acid composition, and Na+,K(+)-ATPase were analyzed in hepatocyte membranes.
Results:
Bile acid secretion and basal and stimulated bile flow were similar in control and UDCA-treated animals but reduced to < 50% in the TPN group. Bile acid-dependent and -independent bile flow were lower in the TPN group. UDCA did not normalize abnormalities in TPN-induced bile composition. Sinusoidal but not canalicular membrane fluidity was different in TPN than in control and UDCA-treated animals. UDCA also increased Na+,K(+)-ATPase activity. Bile and membrane phospholipid fatty acids reflected dietary fatty acids.
Conclusions:
Intravenous UDCA improves bile flow and reduces bilirubin levels in the serum and liver in piglets with TPN-induced cholestasis.
