Wong Weng-Yew, Ward Leigh C, Fong Chee Wai, Yap Wei Ney, Brown Lindsay
School of Biomedical Sciences, University of Queensland, Brisbane, QLD, 4072, Australia.
Laboratory of Cardiovascular Signalling, Centenary Institute, Sydney, NSW, 2050, Australia.
Eur J Nutr. 2017 Feb;56(1):133-150. doi: 10.1007/s00394-015-1064-1. Epub 2015 Oct 8.
This study tested the hypothesis that γ- and δ-tocotrienols are more effective than α-tocotrienol and α-tocopherol in attenuating the signs of diet-induced metabolic syndrome in rats.
Five groups of rats were fed a corn starch-rich (C) diet containing 68 % carbohydrates as polysaccharides, while the other five groups were fed a diet (H) high in simple carbohydrates (fructose and sucrose in food, 25 % fructose in drinking water, total 68 %) and fats (beef tallow, total 24 %) for 16 weeks. Separate groups from each diet were supplemented with either α-, γ-, δ-tocotrienol or α-tocopherol (85 mg/kg/day) for the final 8 of the 16 weeks.
H rats developed visceral obesity, hypertension, insulin resistance, cardiovascular remodelling and fatty liver. α-Tocopherol, α-, γ- and δ-tocotrienols reduced collagen deposition and inflammatory cell infiltration in the heart. Only γ- and δ-tocotrienols improved cardiovascular function and normalised systolic blood pressure compared to H rats. Further, δ-tocotrienol improved glucose tolerance, insulin sensitivity, lipid profile and abdominal adiposity. In the liver, these interventions reduced lipid accumulation, inflammatory infiltrates and plasma liver enzyme activities. Tocotrienols were measured in heart, liver and adipose tissue showing that chronic oral dosage delivered tocotrienols to these organs despite low or no detection of tocotrienols in plasma.
In rats, δ-tocotrienol improved inflammation, heart structure and function, and liver structure and function, while γ-tocotrienol produced more modest improvements, with minimal changes with α-tocotrienol and α-tocopherol. The most important mechanism of action is likely to be reduction in organ inflammation.
本研究检验了以下假设:在减轻大鼠饮食诱导的代谢综合征体征方面,γ-生育三烯酚和δ-生育三烯酚比α-生育三烯酚和α-生育酚更有效。
五组大鼠喂食富含玉米淀粉的(C)饮食,其中68%的碳水化合物为多糖,而其他五组大鼠喂食高糖(食物中含有果糖和蔗糖,饮用水中含有25%的果糖,总计68%)和高脂肪(牛脂,总计24%)的饮食,持续16周。在16周的最后8周,从每种饮食的单独分组中补充α-、γ-、δ-生育三烯酚或α-生育酚(85毫克/千克/天)。
H组大鼠出现内脏肥胖、高血压、胰岛素抵抗、心血管重塑和脂肪肝。α-生育酚、α-、γ-和δ-生育三烯酚减少了心脏中的胶原蛋白沉积和炎症细胞浸润。与H组大鼠相比,只有γ-和δ-生育三烯酚改善了心血管功能并使收缩压恢复正常。此外,δ-生育三烯酚改善了葡萄糖耐量、胰岛素敏感性、血脂谱和腹部肥胖。在肝脏中,这些干预措施减少了脂质积累、炎症浸润和血浆肝酶活性。在心脏、肝脏和脂肪组织中测量了生育三烯酚,结果表明,尽管血浆中生育三烯酚含量低或未检测到,但长期口服给药可将生育三烯酚输送到这些器官。
在大鼠中,δ-生育三烯酚改善了炎症、心脏结构和功能以及肝脏结构和功能,而γ-生育三烯酚的改善作用较小,α-生育三烯酚和α-生育酚的变化最小。最重要的作用机制可能是减少器官炎症。