1Clinical Chemistry Laboratory,Diagnostic Department,ASST Spedali Civili di Brescia,P. Le Spedali Civili 1, 25123 Brescia,Italy.
3Istituto Zooprofilattico Sperimentale della Lombardia e dell'Emilia Romagna (IZSLER),"Bruno Ubertini", Via Bianchi, 9, 25124 Brescia,Italy.
Br J Nutr. 2018 Oct;120(7):751-762. doi: 10.1017/S0007114518001824. Epub 2018 Aug 14.
7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the corresponding Picea abies extract (total extract P. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (-11 and -13 %) and fat mass (-11 and -18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and -12 % smaller and the liver was less steatotic (-62 and -65 %). Serum lipids decreased in TEP-treated mice (-11 % cholesterol, -23 % LDL and -15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genes PPARγ, C/EBPα and aP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1-6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptake in vitro.
7-羟基马替林(7-HMR)是一种植物木质素,在各种植物性食物中以不同浓度存在。本研究旨在测试 7-HMR 的纯化形式 HMRLignan™和相应的云杉 abies 提取物(总提取物 P. abies;TEP)作为膳食补充剂,对高脂肪饮食(HFD)诱导的代谢综合征小鼠和 3T3-L1 脂肪生成模型的影响。3 周龄的小鼠喂食 HFD 60 d。亚组通过口服给予 3 毫克/千克体重 7-HMR(HMRLignan™)或 10 毫克/千克体重 TEP 进行治疗。7-HMR 和 TEP 限制了 HFD 喂养小鼠体重(-11%和-13%)和脂肪量(-11%和-18%)的增加。附睾脂肪细胞分别缩小 19%和-12%,肝脏脂肪变性减少-62%和-65%。TEP 治疗小鼠的血清脂质降低(胆固醇降低-11%,LDL 降低-23%,TAG 降低-15%),两种木质素制剂改善了糖代谢,胰岛素分泌和胰岛素抵抗降低了 70%以上。HFD 调节了几种代谢基因的表达,而木质素则逆转了这种作用。在 3T3-L1 细胞中,7-HMR 代谢物恩诺醇(ENL)和肠二醇(END)对细胞分化的抑制率达到 40%,同时抑制了脂肪生成基因 PPARγ、C/EBPα 和 aP2 的表达。此外,END 和 ENL 导致 HEPA 1-6 肝癌细胞中 TAG 摄取减少 10%。总之,7-HMR 和 TEP 可减轻雄性小鼠代谢综合征和肥胖的代谢失衡,而其代谢物可抑制体外脂肪生成和脂质摄取。