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Delta‐Tocotrienol Dose‐Dependently Decreased Adiposity and Inflammation and Increased Markers of Lipid Oxidation in High Fat Fed Mice

Obesity is a disease that affects one in three American adults. Inflammation has been established as a major underlying basis for obesity and related chronic disorders. Several plant bioactive compounds with anti‐inflammatory properties have been used to reduce obesity and associated metabolic complications. Hence we are investigating the effect of delta‐tocotrienol (δT3), a member of the vitamin E family as an anti‐obesity agent. We hypothesize that δT3 will reduce obesity and insulin resistance through its anti‐inflammatory and anti‐oxidant properties. To test our hypothesis, we used C57BL/6J male mice that were fed a high fat diet (HF) with and without supplementation of increasing levels of delta‐tocotrienol (HF+δT3) up to 1,600mg/kg for 14 weeks. Glucose and insulin tolerance tests were administered two weeks prior to the end of treatments. Serum and tissues including adipose tissue were collected at the end of the study. Our results show significant improvements in glucose clearance in the δT3‐supplemented groups compared to the HF group. Fat pad weights were reduced dose‐dependently by δT3. These changes were also associated with smaller fat cell size and reduced crown like structures macrophages in adipose tissue histology sections from HF+δT3 compared to HF‐ fed mice. We also performed mechanistic analyses that revealed reduction of mRNA and protein expression of pro‐inflammatory adipokines (e.g. resistin, leptin, and MCP‐1) and increased expression of anti‐inflammatory adipokines (e.g. adiponectin and IL‐10 in HF+δT3 compared to HF‐fed mice. Moreover, δT3 dose‐dependently increase fatty acid oxidizing gene. In summary, dietary delta‐tocotrienol exerted promising anti‐obesity and anti‐inflammatory effects that may be mediated in part by adipose tissue.