Aluminum Exposure from Parenteral Nutrition: Early Bile Canaliculus Changes of the Hepatocyte

Amanda R Hall1, Ha Le2, Chris Arnold3

  • 1Department of Surgery, University of Saskatchewan, Saskatoon, SK S7N 5A2, Canada. arb743@mail.usask.ca.

Nutrients
|June 6, 2018
PubMed

Insights

Aluminum in parenteral nutrition (PN) may harm liver cells in neonates. This study found that higher aluminum levels in PN caused structural changes in piglet hepatocytes, potentially impairing bile flow.

Area of Science:

  • Hepatology
  • Neonatal Medicine
  • Toxicology

Background:

  • Parenteral nutrition-associated liver disease (PNALD) affects neonates requiring long-term parenteral nutrition (PN).
  • Aluminum (Al) contamination in infant PN is a concern.
  • Aluminum's role in PNALD pathogenesis is hypothesized but not fully understood.

Purpose of the Study:

  • To investigate the impact of aluminum exposure on hepatocytes in a neonatal piglet model.
  • To determine if aluminum in PN contributes to parenteral nutrition-associated liver disease.

Main Methods:

  • A randomized control trial was conducted using Yucatan piglets (3-6 days old) receiving PN.
  • Two groups were established: high Al (63 µg/kg/day) and low Al (24 µg/kg/day).
  • Serum total bile acids (TBA) were monitored, and liver tissue was analyzed using transmission electron microscopy (TEM) for bile canaliculus morphometry.

Main Results:

  • Piglets receiving high Al PN exhibited smaller bile canalicular spaces compared to the low Al group.
  • High Al exposure resulted in shorter microvilli in the bile canaliculi.
  • Serum TBA levels did not differ significantly between the high and low Al groups.

Conclusions:

  • Aluminum exposure in PN induces structural alterations in hepatocytes, specifically affecting bile canaliculi.
  • Shortened microvilli in hepatocytes due to high Al may reduce the functional area for bile excretion.
  • These structural changes suggest a mechanism by which aluminum could impair bile flow and contribute to PNALD.

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