{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T12:54:08Z","timestamp":1792068848390,"version":"4.4.0"},"reference-count":80,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T00:00:00Z","timestamp":1772668800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Nutr."],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      The aim of the present study was to analyze the effects of an Astaxanthin (ASTX)- rich extract\u2014a powerful antioxidant\u2014obtained from freshwater crustaceans (\n                      <jats:italic>Dilocarcinus pagei<\/jats:italic>\n                      crabs) on liver disturbed lipid metabolism and oxidative stress in rats fed a high-sucrose diet (HSD).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Male Wistar rats were fed for 13 weeks with either: 1\u2014a standard commercial rodent diet (RD), 2\u2014a HSD, 3\u2014a RD plus ASTX, or 4\u2014a HSD plus ASTX. The rats were given orally either ASTX (10 mg\/kg body weight\/day in sunflower oil) or only the vehicle.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>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 \u03b2-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-NF\u03baB p65 protein expression, key transcription factors that govern cellular responses under pro-oxidant and pro-inflammatory conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      This study suggests that ASTX obtained from the freshwater crustacean\n                      <jats:italic>D. pagei<\/jats:italic>\n                      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.\n                    <\/jats:p>\n                  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