Hydroxytyrosol supplementation ameliorates the metabolic disturbances in white adipose tissue from mice fed a high-fat diet through recovery of transcription factors Nrf2, SREBP-1c, PPAR-γ and NF-κB - 09/12/18
, Alejandra Espinosa c, Francisca Echeverría b, Sandra Soto-Alarcon b, Macarena Ortiz d, Luis A. Videla eBienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
Highlights |
• | High-fat diet (HFD) causes white adipose tissue (WAT) hypertrophy, oxidative damage, and depletion of antioxidant defenses. |
• | HFD decreases n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFA), increases lipogenesis and pro-inflammatory status. |
• | Hydroxytyrosol (HT) supplementation attenuates HFD-induced WAT metabolic impairment. |
• | HT improves WAT dysfunction through NF-κΒ, Nrf2, SREBP-1c and PPAR-γ modulation. |
Abstract |
Background |
White adipose tissue (WAT) have a relevant metabolic and inflammatory function, in overweight or obesity conditions. In this regard, the WAT under over feeding nutrition present a significant increment in oxidative stress, pro-inflammatory status and depletion of n-3 long chain polyunsaturated fatty acid. Hydroxytyrosol (HT) is a polyphenol with important cytoprotective effects, and this molecule can modulate the gene expression, transcription factors and enzymatic activity.
Objective |
Therefore, the purpose of this study was evaluate the anti-inflammatory, anti-oxidant and anti-lipogenic effects of HT supplementation mice and the molecular adaptations involved, on dysfunctional WAT from high-fat diet (HFD)-fed mice.
Methods and results |
Male C57BL/6 J mice received (i) control diet (10% fat); (ii) control diet + HT (daily doses of 5 mg kg body weight), (iii) HFD (60% fat); or (iv) HFD + HT for 12 weeks. HFD-fed mice exhibited: (i) WAT hypertrophy; (ii) oxidative stress and depletion of antioxidant defenses, (iii) increased lipogenesis and pro-inflammatory status, (iv) depletion of n-3 LCPUFA and (v) up-regulation of NF-κB and SREBP 1c with down-regulation Nrf2, and PPAR-γ. HT supplementation attenuated the metabolic impairment produced by HFD in WAT, attenuating increment of NF-κB and SREBP 1c, and increasing the activity of Nrf2 and PPAR-γ.
Conclusion |
Supplementation with HT improve the WAT dysfunction induced by HDF in mice through the modulation of transcription factors NF-κB, Nrf2, SREBP-1c and PPAR-γ as well as their target genes, involved in inflammation, antioxidant defenses and lipogenesis.
Le texte complet de cet article est disponible en PDF.Keywords : White adipose tissue, Hydroxytyrosol, Oxidative stress, Nrf2, PPAR-γ, NF-κB
Plan
Vol 109
P. 2472-2481 - janvier 2019 Retour au numéro
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