Weng-Yew Wong1,2, Leigh C Ward3, Chee Wai Fong4, Wei Ney Yap4, Lindsay Brown5. 1. School of Biomedical Sciences, University of Queensland, Brisbane, QLD, 4072, Australia. 2. Laboratory of Cardiovascular Signalling, Centenary Institute, Sydney, NSW, 2050, Australia. 3. School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, 4072, Australia. 4. Davos Life Science Pte Ltd, 3 Biopolis Drive, #04-19 Synapse, Singapore, 138623, Singapore. 5. School of Health and Wellbeing, University of Southern Queensland, Toowoomba, QLD, 4350, Australia. Lindsay.Brown@usq.edu.au.
Abstract
PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
Authors: Jan Frank; Xiao Wei Dawn Chin; Charlotte Schrader; Gunter P Eckert; Gerald Rimbach Journal: Ageing Res Rev Date: 2011-07-07 Impact factor: 10.895
Authors: Marwa E Abdelmageed; George S Shehatou; Rami A Abdelsalam; Ghada M Suddek; Hatem A Salem Journal: Naunyn Schmiedebergs Arch Pharmacol Date: 2018-11-20 Impact factor: 3.000
Authors: Marcus O W Grimm; Liesa Regner; Janine Mett; Christoph P Stahlmann; Pascal Schorr; Christopher Nelke; Olga Streidenberger; Hannah Stoetzel; Jakob Winkler; Shatha R Zaidan; Andrea Thiel; Kristina Endres; Heike S Grimm; Dietrich A Volmer; Tobias Hartmann Journal: Int J Mol Sci Date: 2016-10-29 Impact factor: 5.923