Cyanidin and delphinidin modulate inflammation and altered redox signaling improving insulin resistance in high fat-fed mice.
Cyanidin and delphinidin modulate inflammation and altered redox signaling improving insulin resistance in high fat-fed mice.
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DOI：
10.1016/j.redox.2018.05.012
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发表时间：
2018-09
期刊：
影响因子：
11.4
通讯作者：
Oteiza PI
中科院分区：
文献类型：
--
作者：
Daveri E;Cremonini E;Mastaloudis A;Hester SN;Wood SM;Waterhouse AL;Anderson M;Fraga CG;Oteiza PI
摄入高脂肪和/或果糖含量的饮食会促进组织炎症、氧化应激和胰岛素抵抗，激活信号(例如，核因子-κB/JNK)，下调胰岛素级联反应。目前的证据支持这样的概念，即选择类黄酮可以减轻肥胖和2型糖尿病(T2D)。这项工作调查了补充花青素(AC)、花青素和飞毛虫是否可以减轻小鼠摄入高脂肪饮食(HFD)的不良后果。食用富含AC的混合物可以减轻HFD引起的肥胖、血脂异常和胰岛素抵抗(对胰岛素和葡萄糖的反应受损)。高脂饲料喂养的小鼠的特点是肝脏脂肪沉积和炎症增加，补充AC后这些也得到缓解。HFD导致肝脏氧化应激，表现为NADPH氧化酶表达增加，产生超氧化物和过氧化氢，以及高水平的氧化脂质-蛋白质加合物。这与氧化还原敏感信号IKK/NF-κB和JNK1/2的激活以及由NF-κB调节的PTP1B磷酸酶的表达增加有关，这些都是已知的胰岛素途径的抑制物。与改善胰岛素敏感性相一致的是，补充AC抑制了氧化应激、核因子-PTP1B和κ的激活以及PTP1B的过度表达。因此，通过饮食或补充摄入花青素和飞雀素可能是控制西式饮食不良影响的积极策略，包括超重、肥胖和T2D。炎症、氧化应激和核因子-κB/jnk活化的调节成为AC有益作用的相关靶点。花青素(AC)可减轻高脂饮食(HFD)诱导的小鼠肥胖和胰岛素抵抗。AC可抑制HFD诱导的肝脏脂质沉积和炎症反应。AC可抑制HFD诱导的肝脏NADPH氧化酶上调和氧化应激。AC抑制氧化还原敏感信号的激活，而氧化还原敏感信号会导致胰岛素抵抗。AC可能有益于对抗西式饮食的不利影响。
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 upon AC supplementation. HFD caused liver oxidative stress showing an increased expression of NADPH oxidases, generators of superoxide and H2O2, 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. Anthocyanidins (AC) mitigate high fat diet (HFD)-induced obesity and insulin resistance in mice. AC inhibits HFD-induced liver lipid deposition and inflammation. AC inhibit HFD-induced liver NADPH oxidase upregulation and oxidative stress. AC inhibit the activation of redox sensitive signals that cause insulin resistance. AC could be beneficial against the adverse effects of Western style diets.
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花色苷Delphinidin 3-鲁丁苷刺激通过Ca2+/钙调蛋白依赖性激酶II途径刺激鼠谷物细胞系中胰高血糖素样肽-1分泌。
影响因子：
3.7
作者：
Kato M;Tani T;Terahara N;Tsuda T
通讯作者：
Tsuda T
DOI：
10.1016/j.tem.2012.11.008
发表时间：
2013-02
期刊：
Trends in endocrinology and metabolism: TEM
影响因子：
--
作者：
Dailey MJ;Moran TH
通讯作者：
Moran TH
影响因子：
7.4
作者：
de Ferrars, Rachel M.;Czank, Charles;Kay, Colin D.
通讯作者：
Kay, Colin D.
影响因子：
64.8
作者：
Houstis, N;Rosen, ED;Lander, ES
通讯作者：
Lander, ES
影响因子：
5.2
作者：
Kay, Colin D.;Kroon, Paul A.;Cassidy, Aedin
通讯作者：
Cassidy, Aedin