Vitamin A deficiency injures liver parenchyma and alters the expression of hepatic extracellular matrix.
Vitamin A is an essential lipid-soluble nutrient that is crucial for morphogenesis and adult tissue maintenance. The retinoid homeostasis in the liver depends on a regular supply of vitamin A from an adequate dietary intake to preserve the normal organ structure and functions. This study focuses on the effect of vitamin A deficiency on the morphology and extracellular proteins expression of the liver in adult Wistar rats. Animals were fed with a normal (control group) or deficient vitamin A diet for 3 months. At the end of the experimental period, histological examination of the livers under light and electron microscopy revealed that vitamin A deficiency produced a loss of hepatocyte cord disposition with an irregular parenchymal organization. Abundant fat droplets were present in the cytoplasm of the hepatocytes. Elongated myofibroblastic-like cells with an irregular cytoplasmic process and without lipid droplets could be seen at the perisinusoidal space, where an elevated intensity of alpha smooth muscle actin (alpha-SMA) was observed. These results suggest that an activation of hepatic stellate cells (HSCs) occurred. Moreover, immunochemical methods revealed that vitamin A deficiency led to an increased expression of hepatic fibronectin, laminin and collagen type IV. We propose that vitamin A deprivation caused liver injury and that HSCs underwent a process of activation in which they produced alpha-SMA and synthesized extracellular components. These changes may be a factor predisposing to liver fibrosis. In consequence, vitamin A deprivation could affect human and animal health.
Aguilar
Rossana Pérez
RP
Departamento de Biología del Desarrollo, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) y Universidad Nacional de Tucumán, 4000 San Miguel de Tucumán, Argentina. ssanchez@fbqf.unt.edu.ar
Genta
Susana
S
Oliveros
Liliana
L
Anzulovich
Ana
A
Giménez
María Sofía
MS
Sánchez
Sara S
SS
D000199:Actins / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D024141:Collagen Type IV / Q000378:metabolism / Q000648:ultrastructure; D005109:Extracellular Matrix / Q000378:metabolism* / Q000648:ultrastructure; D005260:Female; D005353:Fibronectins / Q000378:metabolism / Q000648:ultrastructure; D005355:Fibrosis / Q000473:pathology; D022781:Hepatocytes / Q000473:pathology* / Q000648:ultrastructure; D007150:Immunohistochemistry; D007797:Laminin / Q000378:metabolism / Q000648:ultrastructure; D008099:Liver / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014802:Vitamin A Deficiency / Q000473:pathology*
D000199:Actins; D024141:Collagen Type IV; D005353:Fibronectins; D007797:Laminin