Graduate School of Master Program in Anti-Aging and Aesthetic Medicine, Faculty of Medicine, Universitas Padjadjaran, Kabupaten Sumedang, West Java, Indonesia.
Physiology Division, Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Jl. Raya Bandung-Sumedang, KM.21, Hegarmanah, Kec. Jatinangor, Kabupaten Sumedang, West Java, 45363, Indonesia.
Biol Trace Elem Res. 2024 Jun;202(6):2419-2441. doi: 10.1007/s12011-023-03854-2. Epub 2023 Sep 27.
Brown adipose tissue (BAT) and white adipose tissue (WAT) are known to regulate lipid metabolism. A lower amount of BAT compared to WAT, along with adipose tissue dysfunction, can result in obesity. Studies have shown that selenium supplementation protects against adipocyte dysfunction, decreases WAT triglycerides, and increases BAT triiodothyronine (T). In this review, we discuss the relationship between selenium and lipid metabolism regulation through selenoprotein deiodinases and the role of deiodinases and thyroid hormones in the induction of adipose tissue thermogenesis. Upon 22 studies included in our review, we found that studies investigating the relationship between selenium and deiodinases demonstrated that selenium supplementation affects the iodothyronine deiodinase 2 (DIO2) protein and the expression of its associated gene, DIO2, proportionally. However, its effect on DIO1 is inconsistent while its effect on DIO3 activity is not detected. Studies have shown that the activity of deiodinases especially DIO2 protein and DIO2 gene expression is increased along with other browning markers upon white adipose tissue browning induction. Studies showed that thermogenesis is stimulated by the thyroid hormone T as its activity is correlated to the expression of other thermogenesis markers. A proposed mechanism of thermogenesis induction in selenium supplementation is by autophagy control. However, more studies are needed to establish the role of T and autophagy in adipose tissue thermogenesis, especially, since some studies have shown that thermogenesis can function even when T activity is lacking and studies related to autophagy in adipose tissue thermogenesis have contradictory results.
棕色脂肪组织（BAT）和白色脂肪组织（WAT）被认为可以调节脂质代谢。与 WAT 相比，BAT 含量较低，加上脂肪组织功能障碍，可能导致肥胖。研究表明，硒补充剂可以预防脂肪细胞功能障碍，减少 WAT 甘油三酯，增加 BAT 三碘甲状腺原氨酸（T）。在这篇综述中，我们讨论了硒通过硒蛋白脱碘酶与脂质代谢调节的关系，以及脱碘酶和甲状腺激素在诱导脂肪组织产热中的作用。在我们的综述中包括了 22 项研究，我们发现，研究硒与脱碘酶之间关系的研究表明，硒补充剂影响碘甲状腺原氨酸脱碘酶 2（DIO2）蛋白及其相关基因 DIO2 的表达，呈比例关系。然而，其对 DIO1 的影响并不一致，而对 DIO3 活性的影响则检测不到。研究表明，脱碘酶的活性，特别是 DIO2 蛋白和 DIO2 基因表达，随着白色脂肪组织褐变诱导，其他褐变标志物的增加而增加。研究表明，甲状腺激素 T 的活性与其他产热标志物的表达相关，从而刺激产热。硒补充诱导产热的一种假设机制是通过自噬控制。然而，还需要更多的研究来确定 T 和自噬在脂肪组织产热中的作用，特别是因为一些研究表明，即使缺乏 T 活性，产热也可以发挥作用，并且与脂肪组织产热相关的自噬研究结果存在矛盾。
