Shin Su-Kyung, Kwon Eun-Young
Department of Food Science and Nutrition, Kyungpook National University, Daegu 41566, Korea.
Center for Food and Nutritional Genomics Research, Kyungpook National University, Daegu 41566, Korea.
Nutr Res Pract. 2024 Jun;18(3):325-344. doi: 10.4162/nrp.2024.18.3.325. Epub 2024 Apr 22.
BACKGROUND/OBJECTIVES: Kaempferol (Ka) is one of the most widely occurring flavonoids found in large amounts in various plants. Ka has anti-obesity, antioxidant, and anti-inflammatory effects. Despite the numerous papers documenting the efficacy of Ka, some controversy remains. Therefore, this study examined the impact of Ka using 3T3-L1 and high-fat diet-induced obese mice.
MATERIALS/METHODS: 3T3-L1 cells were treated with 50 μM Ka from the initiation of 3T3-L1 differentiation at D0 until the completion of differentiation on D8. Thirty male mice (C57BL/6J, 4 weeks old) were divided into 3 groups: normal diet (ND), high-fat diet (HFD), and HFD + 0.02% (w/w) Ka (Ka) group. All mice were fed their respective diets for 16 weeks. The mice were sacriced, and the plasma and hepatic lipid levels, white adipose tissue weight, hepatic glucose level, lipid level, and antioxidant enzyme activities were analyzed, and immunohistochemistry staining was performed.
Ka suppressed the hypertrophy of 3T3-L1 cells, and the Ka-supplemented mice showed a significant decrease in perirenal, retroperitoneal, mesenteric, and subcutaneous fat compared to the HFD group. Ka supplementation in high-fat diet-induced obese mice also improved the overall blood lipid concentration (total cholesterol, non-high-density lipoprotein-cholesterol, phospholipids, and apolipoprotein B). Ka supplementation in high-fat-induced obesity mice reduced hepatic steatosis and insulin resistance by modulating the hepatic lipid (glucose-6-phosphate dehydrogenase, fatty acid synthase, malic enzyme, phosphatidate phosphohydrolase, and β-oxidation) activities and glucose (glucokinase, phosphoenolpyruvate carboxykinase, and G6pase)-regulating enzymes. Ka supplementation ameliorated the erythrocyte and hepatic mitochondrial HO and inflammation levels (plasma tumor necrosis factor-alpha, monocyte chemoattractant protein-1, interleukin-6, and interferon-gamma and fibrosis of liver and epididymal fat).
Ka may be beneficial for preventing diet-induced obesity, inflammation, oxidative stress, and diabetes.
背景/目的：山奈酚（Ka）是在多种植物中大量广泛存在的黄酮类化合物之一。Ka具有抗肥胖、抗氧化和抗炎作用。尽管有大量文献记载了Ka的功效，但仍存在一些争议。因此，本研究使用3T3-L1细胞和高脂饮食诱导的肥胖小鼠来研究Ka的影响。
材料/方法：从3T3-L1细胞在第0天开始分化直至第8天分化完成，用50μM的Ka处理3T3-L1细胞。将30只雄性小鼠（C57BL/6J，4周龄）分为3组：正常饮食（ND）组、高脂饮食（HFD）组和高脂饮食+0.02%（w/w）Ka（Ka）组。所有小鼠均喂食各自的饮食16周。处死小鼠后，分析血浆和肝脏脂质水平、白色脂肪组织重量、肝脏葡萄糖水平、脂质水平以及抗氧化酶活性，并进行免疫组织化学染色。
Ka抑制了3T3-L1细胞的肥大，与高脂饮食组相比，补充Ka的小鼠肾周、腹膜后、肠系膜和皮下脂肪显著减少。在高脂饮食诱导的肥胖小鼠中补充Ka还改善了总体血脂浓度（总胆固醇、非高密度脂蛋白胆固醇、磷脂和载脂蛋白B）。在高脂诱导的肥胖小鼠中补充Ka通过调节肝脏脂质（葡萄糖-6-磷酸脱氢酶、脂肪酸合酶、苹果酸酶、磷脂酸磷酸水解酶和β-氧化）活性和葡萄糖（葡萄糖激酶、磷酸烯醇式丙酮酸羧激酶和葡萄糖-6-磷酸酶）调节酶来减轻肝脏脂肪变性和胰岛素抵抗。补充Ka改善了红细胞和肝脏线粒体HO以及炎症水平（血浆肿瘤坏死因子-α、单核细胞趋化蛋白-1、白细胞介素-6和干扰素-γ以及肝脏和附睾脂肪的纤维化）。
Ka可能有利于预防饮食诱导的肥胖、炎症、氧化应激和糖尿病。
