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An increase in the number of people with obesity has progressed and obesity leads to the onset of serious diseases such as type-2 diabetes, cardiovascular disease and cancer. Recently, several lines of evidence have suggested that obesity induces neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease which are strongly involved in the dysregulation of brain redox balance. However, there are few drugs to prevent or treat obesity. Therefore, natural compounds such as vitamins and polyphenols are focused on the attenuation of obesity development. Tocotrienols (T3s) belong to one of the vitamin E families. While T3s have antioxidant function, it has been reported that T3s have novel functions such as anti-cancer and neuroprotective functions. From these findings, T3s may have not only antioxidant function but also anti-obesity function. In this paper, we introduce the effects of T3s on obesity progression and obesity-related cognitive dysfunction based on results obtained from our study.

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Vitamin D₃ is metabolized to 25-hydroxyvitamin D₃ (25(OH)D₃) in the liver and further metabolized to 1α,25-dihydroxyvitamin D₃ (1α,25(OH) ₂D₃) in the kidney, which exerts various physiological effects by binding vitamin D receptor (VDR). Both 25(OH)D₃ and 1α,25(OH) ₂D₃ are sequentially metabolized by CYP24A1, resulting in the production of multiple metabolites from them. The reconstituted system using E. coli cells expressing recombinant CYP24A1 is quite useful for the evaluation of vitamin D and its analogs. Using this reconstituted system, we demonstrated that C2-substituted vitamin D analogs were resistant to CYP24A1-dependent catabolism while maintaining high VDR binding affinity. 1α,25(OH) ₂D₃ and its analogs have been clinically used for the rickets. We revealed that daily 25(OH)D₃ administration ameliorated both type I rickets in Cyp27b1 gene-deficient (KO) and type II rickets in mutant Vdr rats without any side effects. We conducted the detailed in vivo metabolic analysis of 25(OH)D₃ using Cyp24a1 KO rats and revealed that not only CYP24A1 but also CYP3A4 played important roles in 25(OH)D₃ metabolism. On the other hand, daily administration of 25(OH)D₃ to Cyp24a1 KO rats caused ectopic calcification and significant weight loss, whereas the same administration to wild type rats caused no side effects. These results suggest that to check the dysfunction of CYP24A1 in advance would be important for the safe intake of vitamin D₃ or 25(OH)D₃.

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