1. Suppression of Lipid Accumulation in 3T3-L1 Adipocytes by α-Tocopheryl Succinate
- Author
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Ryosuke Mitsuhashi, Kentaro Kogure, Dai Majima, Kazuaki Kajimoto, Tatsuya Fukuta, and Misaki Yamasaki
- Subjects
0301 basic medicine ,anti-obesity ,Lipolysis ,alpha-Tocopherol ,Pharmaceutical Science ,adipocyte ,Antioxidants ,Mice ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,3T3-L1 Cells ,Adipocyte ,Adipocytes ,Animals ,Protein kinase A ,Protein kinase B ,Fatty acid synthesis ,Pharmacology ,Dose-Response Relationship, Drug ,Lipogenesis ,3T3-L1 ,Lipid metabolism ,3T3 Cells ,General Medicine ,Sterol regulatory element-binding protein ,030104 developmental biology ,Biochemistry ,chemistry ,030220 oncology & carcinogenesis ,tocopheryl succinate - Abstract
Obesity is a pathological state related to various lifestyle-related diseases, such as diabetes and dyslipidemia, that may be prevented through the development of anti-obesity treatments. Lipid accumulation in cells could be affected by vitamin E ester α-tocopheryl succinate (TS), which has various biological activities, such as anti-cancer effect, via activation of cell signaling pathways, although the antioxidative activity of TS is lost due to esterification of the phenolic OH group. In this study, we found for the first time that TS significantly suppressed lipid accumulation in mouse 3T3-L1 adipocytes. TS treatment reduced the amount of triglycerides in the culture medium, and inhibited activity of glycerol-3-phosphate dehydrogenase, a marker of lipid synthesis. Furthermore, TS accelerated lipolysis. Treatment of adipocytes with TS for 24 h induced no significant cytotoxicity. In TS-treated cells, phosphorylation of Akt, which is involved in fatty acid synthesis via sterol regulatory element-binding proteins (SREBP), was prevented, while levels of phosphorylated protein kinase A (PKA) did not change. Taken together, these results suggest that vitamin E ester TS can suppress lipid accumulation in adipocytes by regulating lipid metabolic cell signaling.
- Published
- 2021