Abstract
Background: Neonates on long-term parenteral nutrition (PN) may develop parenteral nutrition-associated liver disease (PNALD). Aluminum (Al) is a known contaminant of infant PN, and we hypothesize that it substantially contributes to PNALD. In this study, we aim to assess the impact of Al on hepatocytes in a piglet model. Methods: We conducted a randomized control trial using a Yucatan piglet PN model. Piglets, aged 3–6 days, were placed into two groups. The high Al group (n = 8) received PN with 63 µg/kg/day of Al, while the low Al group (n = 7) received PN with 24 µg/kg/day of Al. Serum samples for total bile acids (TBA) were collected over two weeks, and liver tissue was obtained at the end of the experiment. Bile canaliculus morphometry were studied by transmission electron microscopy (TEM) and ImageJ software analysis. Results: The canalicular space was smaller and the microvilli were shorter in the high Al group than in the low Al group. There was no difference in the TBA between the groups. Conclusions: Al causes structural changes in the hepatocytes despite unaltered serum bile acids. High Al in PN is associated with short microvilli, which could decrease the functional excretion area of the hepatocytes and impair bile flow.
Highlights
The typical premature infant receiving parenteral nutrition (PN) is exposed to Al in amounts that far exceed safe limits [1,2]
The measurements obtained from the transmission electron microscopy were compared between the groups using T-tests and Chi-square
The area and the perimeter length of the space was significantly smaller in the high Al (HiAl) as compared to the LoAl group, with mean
Summary
The typical premature infant receiving parenteral nutrition (PN) is exposed to Al in amounts that far exceed safe limits [1,2]. This exposure is further aggravated by the reduced Al excretion of their underdeveloped kidneys [3,4]. Omega-6 lipids are relatively pro-inflammatory and are speculated to be a major contributing factor to parenteral nutrition-associated liver disease (PNALD). Neonates on long-term parenteral nutrition (PN) may develop parenteral nutrition-associated liver disease (PNALD). We aim to assess the impact of Al on hepatocytes in a piglet model. Piglets, aged 3–6 days, were placed into two groups.
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