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

摘要: 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 cascade. Current evidence supports concept select flavonoids can mitigate obesity type 2 diabetes (T2D). This work investigated if supplementation with anthocyanidins (AC) cyanidin delphinidin could attenuate adverse consequences consuming a diet (HFD) mice. an AC-rich blend mitigated HFD-induced obesity, dyslipidemia resistance (impaired responses to glucose). HFD-fed mice were characterized by increased liver lipid deposition which also attenuated upon AC supplementation. HFD caused stress showing expression NADPH oxidases, generators superoxide H2O2, levels oxidized lipid-protein adducts. was associated activation redox sensitive IKK/NF-κB JNK1/2, NF-κB-regulated PTP1B phosphatase, all known inhibitors pathway. In agreement improved sensitivity, inhibited NF-κB JNK activation, overexpression. Thus, consumption either through or be positive strategy control effects Western style diets, including overweight, T2D. Modulation NF-κB/JNK emerge as relevant targets beneficial actions.