The Role of Fucoxanthin in Non-Alcoholic Fatty Liver Disease

Abstract

Chronic liver disease (CLD) has emerged as a leading cause of human deaths. It caused 1.32 million deaths in 2017, which affected men more than women by a two-to-one ratio. There are various causes of CLD, including obesity, excessive alcohol consumption, and viral infection. Among them, non-alcoholic fatty liver disease (NAFLD), one of obesity-induced liver diseases, is the major cause, representing the cause of more than 50% of cases. Fucoxanthin, a carotenoid mainly found in brown seaweed, exhibits various biological activities against NAFLD. Its role in NAFLD appears in several mechanisms, such as inducing thermogenesis in mitochondrial homeostasis, altering lipid metabolism, and promoting anti-inflammatory and anti-oxidant activities. The corresponding altered signaling pathways are the β3-adorenarine receptor (β3Ad), proliferator-activated receptor gamma coactivator (PGC-1), adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor (PPAR), sterol regulatory element binding protein (SREBP), nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), protein kinase B (AKT), SMAD2/3, and P13K/Akt pathways. Fucoxanthin also exhibits anti-fibrogenic activity that prevents non-alcoholic steatohepatitis (NASH) development.

Keywords: fibrosis; fucoxanthin; lipid; liver; non-alcoholic; obesity; thermogenesis.

Figure 1

Fucoxanthin and its metabolites. (A) Fucoxanthin, (B) fucoxanthinol, and (C) amarouciaxanthin A.

Figure 2

The role of fucoxanthin against NAFLD. Fucoxanthin exhibits anti-inflammatory, anti-obesity, anti-oxidant, and anti-fibrogenic activities and alters lipid metabolism in NAFLD.

Figure 3

Fucoxanthin-induced thermogenic activity. Fucoxanthin induces the activation of UCP-1, leading to browning of white adipose tissues. Uncoupled proton leak will occur instead of coupling with oxidative phosphorylation along with heat release (adapted from Huang, (2022)) [50].

Figure 4

Fucoxanthin alters lipid metabolism. (A) Lipogenesis. Fucoxanthin downregulates acetyl CoA carboxylase and fatty acid synthase in lipogenesis, decreasing the lipid content in the liver. (B) Lipolysis. Fucoxanthin promotes β-oxidation, hence resulting in upregulated lipolysis in the liver. The downward arrow indicates downregulation and the upward arrow indicates upregulation.

Figure 5

Signaling pathways altered by fucoxanthin. Fucoxanthin alters β-3-adrenergic receptor (β3Ad), adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor (PPAR), sterol regulatory element binding protein (SREBP), nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and AKT pathways.