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Modest effect of differential dietary vitamin A intake on the pathogenesis of alcohol-associated liver disease.
Ferdouse, Afroza; Clugston, Robin D.
Afiliación
  • Ferdouse A; Department of Physiology, University of Alberta, Edmonton, Alberta, Canada.
  • Clugston RD; The Group on the Molecular and Cell Biology of Lipids, University of Alberta, Edmonton, Alberta, Canada.
Alcohol Clin Exp Res (Hoboken) ; 48(6): 1036-1049, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38649284
ABSTRACT

BACKGROUND:

Chronic alcohol consumption is a major public health issue. The primary organ damaged by alcohol abuse is the liver, leading to alcohol-associated liver disease (ALD). ALD begins with hepatic steatosis and can progress to fibrosis and cirrhosis; however, we have an incomplete understanding of ALD pathogenesis. Interestingly, the liver is also the major organ for vitamin A metabolism and storage, and ALD has previously been linked with altered hepatic vitamin A homeostasis. We hypothesize that alcohol-induced vitamin A depletion disrupts its normal function in the liver, contributing to the pathogenesis of ALD. To test this hypothesis, we postulated that adding copious vitamin A to the diet might alleviate ALD, and conversely, that a vitamin A deficient diet would worsen ALD.

METHODS:

We conducted two dietary intervention studies in mice comparing deficient (0 IU/g diet) and copious (25 IU/g diet) dietary vitamin A intake versus control (4 IU/g diet), using the NIAAA chronic-binge model of ALD. Hepatic steatosis was assessed using histopathological and biochemical approaches. Tissue Vitamin A levels were measured using high-performance liquid chromatography. Markers of ALD, hepatic inflammation and lipid metabolism were analyzed by the quantitative polymerase chain reaction and western blotting.

RESULTS:

As expected, a 0 IU/g Vitamin A diet decreased, and a 25 IU/g Vitamin A diet increased hepatic Vitamin A stores. However, alcohol induced changes in hepatic triglyceride levels, markers of hepatic lipid metabolism, inflammation and fibrosis were not significantly different in mice consuming a copious or deficient vitamin A diet compared to control.

CONCLUSIONS:

Altered vitamin A intake and hepatic vitamin A storage have a minor effect on the pathogenesis of ALD. Thus, given the known link between altered retinoic acid signaling and ALD, future studies that further explore this linkage are warranted.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Alcohol Clin Exp Res (Hoboken) Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Alcohol Clin Exp Res (Hoboken) Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Estados Unidos