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Cited by 10Liver Disease Diagnosis and TreatmentAntioxidant Activity and Oxidative StressDrug-Induced Hepatotoxicity and Protection

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Prevention of NAFLD/NASH by Astaxanthin and β-Cryptoxanthin

Ota, Tsuguhito·2021·Advances in Experimental Medicine and Biology
DOI 10.1007/978-981-15-7360-6_21
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Abstract

Metabolic disorders, such as lipid accumulation, insulin resistance, and inflammation, have been implicated in the pathogenesis of NAFLD/NASH. Both innate and recruited immune cells mediate the development of insulin resistance and NASH. Oxidative stress is also pivotal for the progression of NASH. Astaxanthin is a natural carotenoid mainly derived from microorganisms and marine organisms. Due to its special chemical structure, astaxanthin has strong antioxidant activity. β-Cryptoxanthin is a xanthophyll carotenoid specifically found in the Satsuma mandarin. β-Cryptoxanthin is readily absorbed and relatively abundant in human plasma, together with α-carotene, β-carotene, lycopene, lutein, and zeaxanthin. Considering the unique chemical properties of astaxanthin and β-cryptoxanthin and the complex pathogenic mechanism of NASH, astaxanthin and β-cryptoxanthin are regarded as a considerable compound for the prevention and treatment of NASH. This chapter comprehensively describes the mechanism of the application for astaxanthin and β-cryptoxanthin on the prevention and treatment of NASH from the aspects, including antioxidative stress, inhibition of inflammation and promotion of M2 macrophage polarization, improvement of mitochondrial oxidative respiration, amelioration of insulin resistance, and suppression of fibrosis.

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  • Improved mitochondrial function, including enhanced oxidative phosphorylation and mitochondrial biogenesis, is consistently associated with macrophage reprogramming and fibrosis resolution.

    “Conversely, improved mitochondrial function -including enhanced oxidative phosphorylation and mitochondrial biogenesis- has been consistently associated with macrophage reprogramming and fibrosis resolution (28–31).”

    From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [29]

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Metadata

Authors
Ota, T.
Affiliations
Kanazawa University (JP)
Corresponding author
Ota, Tsuguhito
ORCID
Ota, Tsuguhito
Venue
Advances in Experimental Medicine and Biology
Publisher
Springer Singapore
Published
2021
Volume
1261
Pages
231-238
ISSN
  • 0065-2598 (ISSN-L)
  • 2214-8019
DOI
10.1007/978-981-15-7360-6_21
OpenAlex
W3143305469
Cited by
10
References
1
Citations by year
2026: 1 · 2025: 2 · 2023: 5 · 2021: 2
FWCI
10.05
Type
book chapter
Language
en
Open access
closed
Licence
Locations
  • Advances in experimental medicine and biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Keywords
non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, astaxanthin, beta-cryptoxanthin, carotenoids, oxidative stress, antioxidant activity, inflammation, M2 macrophage polarization, insulin resistance, mitochondrial respiration, liver fibrosis, lipid accumulation
MeSH terms
Beta-Cryptoxanthin, Antioxidants, Humans, Xanthophylls, Non-alcoholic Fatty Liver Disease

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