# Astaxanthin alleviates altered hepatic lipid metabolism and oxidative stress in animals fed a high-sucrose diet

**Authors:** Matias Rodrigo Vargas, María del Rosario Ferreira, Paola Inés Ingaramo, Pablo Collins, María Eugenia D’Alessandro

PMC · DOI: 10.3389/fnut.2026.1781406 · 2026-03-05

## TL;DR

Astaxanthin from freshwater crabs reduces liver damage and oxidative stress in rats on a high-sucrose diet.

## Contribution

Demonstrates astaxanthin's efficacy in mitigating hepatic lipid metabolism and oxidative stress in high-sucrose-fed rats.

## Key findings

- Astaxanthin reduced liver steatosis and triglyceride accumulation in high-sucrose-fed rats.
- Astaxanthin improved redox status by lowering ROS and increasing antioxidant enzyme activity.
- Astaxanthin modulated Nrf2 and p-NFκB p65, key regulators of oxidative and inflammatory responses.

## Abstract

The aim of the present study was to analyze the effects of an Astaxanthin (ASTX)- rich extract—a powerful antioxidant—obtained from freshwater crustaceans (Dilocarcinus pagei crabs) on liver disturbed lipid metabolism and oxidative stress in rats fed a high-sucrose diet (HSD).

Male Wistar rats were fed for 13 weeks with either: 1—a standard commercial rodent diet (RD), 2—a HSD, 3—a RD plus ASTX, or 4—a HSD plus ASTX. The rats were given orally either ASTX (10 mg/kg body weight/day in sunflower oil) or only the vehicle.

ASTX supplementation attenuated liver injury, as reflected by a reduction in steatosis severity and hepatic triglyceride accumulation. This effect appears to be primarily achieved by promoting mitochondrial fatty acid β-oxidation, as suggested by increased hepatic carnitine palmitoyltransferase-1 (CPT-1) activity, without significantly affecting lipogenesis. In addition, ASTX improved intracellular redox status by preventing the increase in hepatic reactive oxygen species (ROS) levels and by promoting a significant increase in the activity of the antioxidant enzymes catalase (CAT) and glutathione S-transferase (GST). ASTX was also able to restore altered GSH levels. Furthermore, ASTX induced an up-regulation of Nrf2 and a down-regulation of p-NFκB p65 protein expression, key transcription factors that govern cellular responses under pro-oxidant and pro-inflammatory conditions.

This study suggests that ASTX obtained from the freshwater crustacean D. pagei exerts beneficial effects against altered hepatic lipid metabolism and oxidative stress in HSD-fed rats, positioning this species as a promising novel source of ASTX for functional nutrition strategies.

Diagram of a male Wistar rat study comparing high-sucrose diet (HSD) vs HSD plus astaxanthin (ASTX) for 13 weeks (ASTX 10 mg/kg/day). Left (HSD, green) shows increased liver weight, NAS, lipogenic enzyme activity, ROS, GSH, and p NFκB p65, with decreased CPT 1 activity, antioxidant enzyme activity, and Nrf2. Right (HSD+ASTX, red) shows reduced liver weight/NAS and inflammatory/oxidative markers, with improved CPT 1, CAT/GST, and Nrf2.

## Linked entities

- **Proteins:** CPT1A (carnitine palmitoyltransferase 1A), CAT (catalase), SLCO6A1 (solute carrier organic anion transporter family member 6A1), GABPA (GA binding protein transcription factor subunit alpha)
- **Chemicals:** astaxanthin (PubChem CID 5281224)
- **Species:** Dilocarcinus pagei (taxon 169885), Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Cat (catalase) [NCBI Gene 24248] {aka CS1, Cas1, Cat01, Catl, Cs-1}, Hpgds (hematopoietic prostaglandin D synthase) [NCBI Gene 58962] {aka Ptgds2}, Nfe2l2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 83619]
- **Diseases:** inflammatory (MESH:D007249), steatosis (MESH:D005234), liver injury (MESH:D017093)
- **Chemicals:** lipid (MESH:D008055), triglyceride (MESH:D014280), fatty acid (MESH:D005227), sucrose (MESH:D013395), GSH (MESH:D005978), ASTX (MESH:C005948), ROS (MESH:D017382)
- **Species:** crustaceans [taxon 6657], Dilocarcinus pagei (species) [taxon 169885], Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12999564/full.md

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Source: https://tomesphere.com/paper/PMC12999564