Oxidative stress is implicated in the pathogenesis of many diseases including obesity, non-alcoholic fatty liver disease, and diabetes mellitus. Previously, we reported that siphonaxanthin, a carotenoid from green algae, elicited a potent inhibitory effect on hepatic de novo lipogenesis, and an anti-obesity effect in both 3T3L1 cells and KKAy mice. Thus, we hypothesized that consumption of siphonaxanthin could improve metabolic disorders including hepatic steatosis and systemic adiposity, as well as ameliorate somatic stress under obese conditions. Both the hepatocyte cell line HepG2 and a mouse model of severe obesity, produced by feeding Ob/Ob mice on a high-fat diet (HFD), were used to test this hypothesis. In obese mice, siphonaxanthin intake did not improve liver steatosis or systemic adiposity. However, intake did lower plasma glucose and alanine aminotransferase (ALT) levels and diminished hepatic lipid peroxidation products and antioxidant gene expression, which increased significantly in control group obese mice. Renal protein carbonyl content decreased significantly in the siphonaxanthin group, which might also indicate an ameliorated oxidative stress. Siphonaxanthin restored gene expression related to antioxidant signaling, lipid β-oxidation, and endoplasmic-reticulum-associated protein degradation in the kidney, which decreased significantly in obese mice. Liver and kidney responded to obesity-induced somatic stress in a divergent pattern. In addition, we confirmed that siphonaxanthin potently induced Nrf2-regulated antioxidant signaling in HepG2 cells. In conclusion, our results indicated that siphonaxanthin might protect obesity-leading somatic stress through restoration of Nrf2-regulated antioxidant signaling, and might be a promising nutritional supplement.

中文翻译：

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Siphonaxanthin 是一种来自绿藻 Codium cylindricum 的类胡萝卜素，通过改善体细胞应激和恢复抗氧化能力，保护高脂肪饮食喂养的 Ob/Ob 小鼠免受脂毒性

氧化应激与许多疾病的发病机制有关，包括肥胖、非酒精性脂肪肝和糖尿病。以前，我们报道了虹吸黄素，一种来自绿藻的类胡萝卜素，对肝脏从头脂肪生成产生有效的抑制作用，并在 3T3L1 细胞和 KKAy 小鼠中产生抗肥胖作用。因此，我们假设摄入虹吸黄质可以改善代谢紊乱，包括肝脂肪变性和全身性肥胖，以及在肥胖条件下改善躯体压力。肝细胞系 HepG2 和重度肥胖小鼠模型（通过以高脂肪饮食 (HFD) 喂养 Ob/Ob 小鼠产生）都被用于检验这一假设。在肥胖小鼠中，虹吸黄质摄入并没有改善肝脏脂肪变性或全身性肥胖。然而，摄入确实降低了血浆葡萄糖和丙氨酸氨基转移酶 (ALT) 水平，并减少了肝脏脂质过氧化产物和抗氧化基因的表达，这在对照组肥胖小鼠中显着增加。虹吸黄素组的肾蛋白羰基含量显着降低，这也可能表明氧化应激得到改善。虹吸黄质恢复了肾脏中与抗氧化信号、脂质 β-氧化和内质网相关蛋白降解相关的基因表达，在肥胖小鼠中显着降低。肝脏和肾脏以不同的模式对肥胖引起的躯体应激做出反应。此外，我们证实了虹吸黄素在 HepG2 细胞中有效诱导 Nrf2 调节的抗氧化信号。综上所述，