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Abstract Title:

Cyanidin and delphinidin modulate inflammation and altered redox signaling improving insulin resistance in high fat-fed mice.

Abstract Source:

Redox Biol. 2018 May 30 ;18:16-24. Epub 2018 May 30. PMID: 29890336

Abstract Author(s):

Elena Daveri, Eleonora Cremonini, Angela Mastaloudis, Shelly N Hester, Steven M Wood, Andrew L Waterhouse, Mauri Anderson, Cesar G Fraga, Patricia I Oteiza

Article Affiliation:

Elena Daveri

Abstract:

Consumption of diets high in fat and/or fructose content promotes tissue inflammation, oxidative stress, and insulin resistance, activating signals (e.g. NF-κB/JNK) that downregulate the insulin cascade. Current evidence supports the concept that select flavonoids can mitigate obesity and type 2 diabetes (T2D). This work investigated if supplementation with the anthocyanidins (AC) cyanidin and delphinidin could attenuate the adverse consequences of consuming a high fat diet (HFD) in mice. Consumption of an AC-rich blend mitigated HFD-induced obesity, dyslipidemia and insulin resistance (impaired responses to insulin and glucose). HFD-fed mice were characterized by increased liver lipid deposition and inflammation, which were also attenuated uponAC supplementation. HFD caused liver oxidative stress showing an increased expression of NADPH oxidases, generators of superoxide and HO, and high levels of oxidized lipid-protein adducts. This was associated with the activation of the redox sensitive signals IKK/NF-κB and JNK1/2, and increased expression of the NF-κB-regulated PTP1B phosphatase, all known inhibitors of the insulin pathway. In agreement with an improved insulin sensitivity, AC supplementation inhibited oxidative stress, NF-κB and JNK activation, and PTP1B overexpression. Thus, cyanidin and delphinidin consumption either through diet or by supplementation could be a positive strategy to control the adverse effects of Western style diets, including overweight, obesity, and T2D. Modulation of inflammation, oxidative stress, and NF-κB/JNK activation emerge as relevant targets of AC beneficial actions.

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Sayer Ji
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