Vazquez Prieto Marcela A, Bettaieb Ahmed, Rodriguez Lanzi Cecilia, Soto Verónica C, Perdicaro Diahann J, Galmarini Claudio R, Haj Fawaz G, Miatello Roberto M, Oteiza Patricia I
Area de Fisiología Patológica, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, e Instituto de Medicina y Biología Experimental de Cuyo (IMBECU-CONICET), Mendoza, Argentina.
Mol Nutr Food Res. 2015 Apr;59(4):622-33. doi: 10.1002/mnfr.201400631. Epub 2015 Mar 11.
This study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF-α) in 3T3-L1 adipocytes.
In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/day of C, Q, and CQ improved all these parameters. In 3T3-L1 adipocytes, C and Q attenuated TNF-α-induced elevated protein carbonyls, increased proinflammatory cytokine expression (MCP-1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to (i) decrease the activation of the mitogen-activated kinases (MAPKs) JNK and p38; and (ii) prevent the downregulation of PPAR-γ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose proinflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNF-α, MCP-1, resistin) insulin sensitivity.
Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS-associated adipose inflammation, oxidative stress, and insulin resistance.
本研究评估了膳食儿茶素(C)、槲皮素(Q)以及二者组合(CQ)减轻大鼠高果糖(HFr)摄入引发的脂肪炎症以及3T3-L1脂肪细胞中肿瘤坏死因子α(TNF-α)引发的脂肪炎症的能力。
在大鼠中,6周的HFr摄入导致血脂异常、胰岛素抵抗、血浆脂联素降低、肥胖以及脂肪组织炎症。每日补充20 mg/kg的C、Q和CQ可改善所有这些参数。在3T3-L1脂肪细胞中,C和Q减轻了TNF-α诱导的蛋白质羰基升高、促炎细胞因子表达增加(MCP-1、抵抗素)以及脂联素降低。C和Q对脂肪炎症的保护作用部分与其以下能力有关:(i)降低丝裂原活化蛋白激酶(MAPK)JNK和p38的激活;(ii)防止PPAR-γ的下调。总之,C和Q,以及在更大程度上二者的组合,减轻了脂肪促炎信号级联反应,并调节了改善(脂联素)或损害(TNF-α、MCP-1、抵抗素)胰岛素敏感性的分子平衡。
总之,这些发现表明膳食Q和C在减轻与代谢综合征相关的脂肪炎症、氧化应激和胰岛素抵抗方面可能具有潜在益处。