Abstract
The objective of this review is to explore the relationship between alcohol and the metabolism of the essential micronutrient, vitamin A; as well as the impact this interaction has on alcohol-induced disease in adults. Depleted hepatic vitamin A content has been reported in human alcoholics, an observation that has been confirmed in animal models of chronic alcohol consumption. Indeed, alcohol consumption has been associated with declines in hepatic levels of retinol (vitamin A), as well as retinyl ester and retinoic acid; collectively referred to as retinoids. Through the use of animal models, the complex interplay between alcohol metabolism and vitamin A homeostasis has been studied; the reviewed research supports the notion that chronic alcohol consumption precipitates a decline in hepatic retinoid levels through increased breakdown, as well as increased export to extra-hepatic tissues. While the precise biochemical mechanisms governing alcohol’s effect remain to be elucidated, its profound effect on hepatic retinoid status is irrefutable. In addition to a review of the literature related to studies on tissue retinoid levels and the metabolic interactions between alcohol and retinoids, the significance of altered hepatic retinoid metabolism in the context of alcoholic liver disease is also considered.
Highlights
The primary pathway for ethanol metabolism in the human body is its oxidative metabolism from ethanol to acetaldehyde, and to acetic acid
Decreased plasma retinol levels and plasma retinol binding protein (RBP) concentrations have been reported in alcoholics by several groups [10,12,13]; it was the landmark 1982 study by Leo and Lieber that established the profound effect that alcohol can have on hepatic vitamin A status [14]
In the toxic burst hypothesis, alcohol-induced aberrations in hepatic retinoid metabolism results in a toxic burst of transcriptionally active retinoid metabolites, presumable generated by cytochrome P450 2E1 (CYP2E1), which directly contribute to the development of alcoholic liver disease [25]
Summary
The primary pathway for ethanol metabolism in the human body is its oxidative metabolism from ethanol to acetaldehyde, and to acetic acid. The metabolism of dietary vitamin A follows a parallel pathway, including the oxidative metabolism of retinol to retinaldehyde, to the canonically active form of vitamin A, retinoic acid (collectively referred to as retinoids; Figure 1) [3]. Given these biochemical parallels, it is perhaps not surprising that ethanol has been shown to negatively affect retinoid homeostasis following both acute and chronic ethanol exposure. The scope of this review includes alcohol’s effect on retinoid metabolism and homeostasis in adult tissues, the liver; it should be noted that ethanol has been proposed to disrupt retinoid signaling during development which has been associated with fetal alcohol syndrome. The synthesis of retinyl ester is catalyzed by lecithin: retinol acyltransferase (LRAT); the molecular identity of enzymes which synthesize fatty acid ethyl esters are currently unknown
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