?-Cryptoxanthin ameliorates metabolic risk factors by regulating NF-?B and Nrf2 pathways in insulin resistance induced by high-fat diet in rodents

dc.contributor.authorŞahin, Kazım
dc.contributor.authorOrhan, Cemal
dc.contributor.authorAkdemir, Fatih
dc.contributor.authorTuzcu, Mehmet
dc.contributor.authorŞahin, Nurhan
dc.contributor.authorYilmaz, Ismet
dc.contributor.authorJuturu, Vijaya
dc.date.accessioned2026-08-12T17:33:20Z
dc.date.issued2017
dc.departmentFırat Üniversitesi
dc.description.abstractThe aim of this experiment was to determine the effects of beta-cryptoxanthin (BCX) on the cardiometabolic health risk factors and NF-kappa B and Nrf2 pathway in insulin resistance induced by high-fat diet (HFD) in rodents. Twenty-eight Sprague-Dawley rats were allocated into four groups: (1) Control, rats fed a standard diet for 12 weeks; (2) BCX, rats fed a standard diet and supplemented with BCX (2.5 mg/kg BW) for 12 weeks; (3) HFD, rats fed a HFD for 12 weeks, (4) HFD + BCX, rats fed a HFD and supplemented with BCX for 12 weeks. BCX reduced cardio-metabolic health markers and decreased inflammatory markers (P < 0.001). Rats fed a HFD had the lower total antioxidant capacity and antioxidant enzymes activities and higher MDA concentration than control rats (P < 0.001 for all). Comparing with the HFD group, BCX in combination with HFD inhibited liver NF-kappa B and TNF-alpha expression by 22% and 14% and enhanced liver Nrf2, HO-1, PPAR-alpha, and p-IRS-1 by 1.43,1.41, 3.53, and 1.33 fold, respectively (P < 0.001). Furthermore, in adipose tissue, BCX up-regulated Nrf2, HO-1, PPAR-alpha, and p-IRS-1 expression, whereas, down-regulated NF-kappa B and TNF-alpha expression. In conclusion, BCX decreased visceral fat and cardiometabolic health risk factors through modulating expressions of nuclear transcription factors. (C) 2017 Elsevier Ltd. All rights reserved.
dc.description.sponsorshipOmniActive Health Technologies Inc. (NJ, USA); Turkish Academy of Sciences
dc.description.sponsorshipThis study was sponsored by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences.
dc.identifier.doi10.1016/j.fct.2017.07.008
dc.identifier.endpage279
dc.identifier.issn0278-6915
dc.identifier.issn1873-6351
dc.identifier.orcid0000-0002-5779-6631
dc.identifier.orcid0000-0003-4138-7689
dc.identifier.orcid0000-0002-1329-3143
dc.identifier.orcid0000-0001-9542-5244
dc.identifier.pmid28689061
dc.identifier.scopus2-s2.0-85021888593
dc.identifier.scopusqualityQ1
dc.identifier.startpage270
dc.identifier.urihttps://doi.org/10.1016/j.fct.2017.07.008
dc.identifier.urihttps://hdl.handle.net/11508/56968
dc.identifier.volume107
dc.identifier.wosWOS:000407982900027
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofFood and Chemical Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectHigh-fat diet
dc.subjectbeta-cryptoxanthin
dc.subjectInflammation
dc.subjectAntioxidant properties
dc.title?-Cryptoxanthin ameliorates metabolic risk factors by regulating NF-?B and Nrf2 pathways in insulin resistance induced by high-fat diet in rodents
dc.typeArticle

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