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Review
. 2016 Jan 6;6(1):1.
doi: 10.3390/biom6010001.

Alcoholic Liver Disease: Update on the Role of Dietary Fat

Irina A Kirpich  1   2 , Matthew E Miller  3 , Matthew C Cave  4   5   6 , Swati Joshi-Barve  7   8 , Craig J McClain  9   10   11
Affiliations
Review

Alcoholic Liver Disease: Update on the Role of Dietary Fat

Irina A Kirpich et al. Biomolecules. .

Abstract

Alcoholic liver disease (ALD) spans a spectrum of liver pathology, including fatty liver, alcoholic steatohepatitis, and cirrhosis. Accumulating evidence suggests that dietary factors, including dietary fat, as well as alcohol, play critical roles in the pathogenesis of ALD. The protective effects of dietary saturated fat (SF) and deleterious effects of dietary unsaturated fat (USF) on alcohol-induced liver pathology are well recognized and documented in experimental animal models of ALD. Moreover, it has been demonstrated in an epidemiological study of alcoholic cirrhosis that dietary intake of SF was associated with a lower mortality rates, whereas dietary intake of USF was associated with a higher mortality. In addition, oxidized lipids (dietary and in vivo generated) may play a role in liver pathology. The understanding of how dietary fat contributes to the ALD pathogenesis will enhance our knowledge regarding the molecular mechanisms of ALD development and progression, and may result in the development of novel diet-based therapeutic strategies for ALD management. This review explores the relevant scientific literature and provides a current understanding of recent advances regarding the role of dietary lipids in ALD pathogenesis.

Keywords: alcoholic liver disease; gut microbiota; oxidized dietary lipids; oxidized linoleic acid metabolites; saturated and unsaturated dietary fat.

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Figures

Figure 1
Figure 1
Omega ω-6 and ω-3 essential fatty acids and their metabolites. Abbreviations: AEA: N-arachidonoylethanolamine (anandamide); 2-AG: 2-arachidonoylglycerol; LXA4: lipoxin A4; LXB4: lipoxin B4; PUFA: polyunsaturated fatty acid.
Figure 2
Figure 2
Oxidative metabolism of linoleic acid. LA can be enzymatically or non-enzymatically converted to 9- and 13-HpODE, with subsequent enzymatic conversion to hydroxy (9- and 13-HODE) and ketone (9- and 13-oxoODE) derivatives. Abbreviations: HpODE: hydroperoxy-octadecadienoic acid; HODE: hydroxy-octadecadienoic acid; oxoODE: oxo-octadecadienoic acid.
Figure 3
Figure 3
Proposed model of OXLAM/TRPV1-mediated mechanism of USF and EtOH-mediated liver injury and inflammation. Abbreviations: EtOH: ethanol; LOX: lypoxygenase; ROS: reactive oxygen species; OXLAMs: oxidized linoleic metabolites; TRPV1: Transient Receptor Potential Vanilloid 1.
Figure 4
Figure 4
Differential effects of dietary saturated and unsaturated fat on EtOH-induced intestinal and liver alterations.
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