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Ethanol Impaired Liver Regeneration is Associated with Decreased Aspartyl‐AsparagylβHydroxylase (AAH) Expression.
Author(s) -
Duan Kevin,
Chaudhry Rajeev,
Pang Maoyin,
Wands Jack,
de la Monte Suzanne
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1136-c
Subject(s) - liver regeneration , endocrinology , medicine , biology , regeneration (biology) , steatosis , gene expression , insulin , microbiology and biotechnology , biochemistry , gene
Insulin and IGF signaling mediate cell growth, differentiation, motility, adhesion, energy metabolism, and gene expression, all of which are required for liver regeneration and impaired by chronic ethanol abuse. Recent studies showed that AAH, a key enzyme that mediates cell growth, motility, and adhesion, is regulated by insulin and IGF. This study utilizes an in vivo model to examine the effects of chronic ethanol feeding on AAH expression in relation to liver regeneration. Adult Long‐Evans rats were fed liquid diets containing 0% or 37% ethanol by caloric content for 5 weeks. Rats were subjected to 70% hepatectomy. Livers were harvested 0–7 days later to characterize AAH expression in relation to liver regeneration. Livers from ethanol fed rats had increased steatosis, disordered lobular architecture, and reduced levels of AAH expression. During regeneration, the peak period of DNA synthesis was delayed and muted in the ethanol‐fed relative to control livers. In addition, AAH gene expression was up‐regulated shortly after the period of maximum DNA synthesis, whereas in the ethanol‐fed group, AAH expression was mainly increased on Day 7 during the period of non‐parenchymal cell proliferation. In conclusion, ethanol impaired liver regeneration and remodeling are associated with decreased AAH expression. Future studies will determine if bolstering AAH expression rescues ethanol‐impaired liver regeneration.