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The adverse effects of alcohol on vitamin A metabolism.

Clugston RD, Blaner WS - Nutrients (2012)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Institute of Human Nutrition, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. rdc2132@columbia.edu

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.

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Biochemical parallels in the metabolism of ethanol and retinol. The conversion of ethanol to acetaldehyde is mediated by different processes within the cell; this reaction can be catalyzed by alcohol dehydrogenase, CYP2E1, and to a lesser extent, catalase. The conversion of the primary alcohol, retinol, to retinaldehyde can also be catalyzed by alcohol dehydrogenase subtypes, as well as specific retinol dehydrogenases. In both cases, the subsequent oxidation of the aldehyde to a carboxylic acid is mediated by aldehyde dehydrogenases. Within the liver, 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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nutrients-04-00356-f001: Biochemical parallels in the metabolism of ethanol and retinol. The conversion of ethanol to acetaldehyde is mediated by different processes within the cell; this reaction can be catalyzed by alcohol dehydrogenase, CYP2E1, and to a lesser extent, catalase. The conversion of the primary alcohol, retinol, to retinaldehyde can also be catalyzed by alcohol dehydrogenase subtypes, as well as specific retinol dehydrogenases. In both cases, the subsequent oxidation of the aldehyde to a carboxylic acid is mediated by aldehyde dehydrogenases. Within the liver, 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.

Mentions: The primary pathway for ethanol metabolism in the human body is its oxidative metabolism from ethanol to acetaldehyde, and then to acetic acid. Furthermore, ethanol can also undergo so called non-oxidative metabolism, which includes the esterification of ethanol into fatty acid ethyl esters, as well as its conversion into phosphatidylethanol [1,2]. Similarly, the metabolism of dietary vitamin A follows a parallel pathway, including the oxidative metabolism of retinol to retinaldehyde, then 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. Indeed, as discussed below, enzymes which are involved in ethanol metabolism are also thought to affect retinoid homeostasis, such as alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1). The scope of this review includes alcohol’s effect on retinoid metabolism and homeostasis in adult tissues, particularly the liver; however, it should be noted that ethanol has also been proposed to disrupt retinoid signaling during development which has been associated with fetal alcohol syndrome. This subject will not be covered in the current review and the reader is directed toward the existing review literature on fetal alcohol syndrome and retinoids [4,5].


The adverse effects of alcohol on vitamin A metabolism.

Clugston RD, Blaner WS - Nutrients (2012)

Biochemical parallels in the metabolism of ethanol and retinol. The conversion of ethanol to acetaldehyde is mediated by different processes within the cell; this reaction can be catalyzed by alcohol dehydrogenase, CYP2E1, and to a lesser extent, catalase. The conversion of the primary alcohol, retinol, to retinaldehyde can also be catalyzed by alcohol dehydrogenase subtypes, as well as specific retinol dehydrogenases. In both cases, the subsequent oxidation of the aldehyde to a carboxylic acid is mediated by aldehyde dehydrogenases. Within the liver, 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.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3367262&req=5

nutrients-04-00356-f001: Biochemical parallels in the metabolism of ethanol and retinol. The conversion of ethanol to acetaldehyde is mediated by different processes within the cell; this reaction can be catalyzed by alcohol dehydrogenase, CYP2E1, and to a lesser extent, catalase. The conversion of the primary alcohol, retinol, to retinaldehyde can also be catalyzed by alcohol dehydrogenase subtypes, as well as specific retinol dehydrogenases. In both cases, the subsequent oxidation of the aldehyde to a carboxylic acid is mediated by aldehyde dehydrogenases. Within the liver, 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.
Mentions: The primary pathway for ethanol metabolism in the human body is its oxidative metabolism from ethanol to acetaldehyde, and then to acetic acid. Furthermore, ethanol can also undergo so called non-oxidative metabolism, which includes the esterification of ethanol into fatty acid ethyl esters, as well as its conversion into phosphatidylethanol [1,2]. Similarly, the metabolism of dietary vitamin A follows a parallel pathway, including the oxidative metabolism of retinol to retinaldehyde, then 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. Indeed, as discussed below, enzymes which are involved in ethanol metabolism are also thought to affect retinoid homeostasis, such as alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1). The scope of this review includes alcohol’s effect on retinoid metabolism and homeostasis in adult tissues, particularly the liver; however, it should be noted that ethanol has also been proposed to disrupt retinoid signaling during development which has been associated with fetal alcohol syndrome. This subject will not be covered in the current review and the reader is directed toward the existing review literature on fetal alcohol syndrome and retinoids [4,5].

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Institute of Human Nutrition, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. rdc2132@columbia.edu

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.

Show MeSH
Related in: MedlinePlus