Department of Nutritional Sciences, University of Vienna, Vienna, Austria.
Institute of Physiological Chemistry, Faculty of Chemistry, University of Vienna, Vienna, Austria; Faculty of Chemistry, Vienna Doctoral School in Chemistry (DoSChem), University of Vienna, Vienna, Austria.
J Nutr Biochem. 2024 Dec;134:109720. doi: 10.1016/j.jnutbio.2024.109720. Epub 2024 Aug 3.
Previously, we demonstrated that caloric restriction (CR) stimulates the synthesis, conjugation, secretion, and deconjugation of taurine and bile acids in the intestine, as well as their reuptake. Given taurine's potent antiobesogenic properties, this study aimed to assess whether the CR-induced shift in taurine homeostasis contributes to adipose tissue loss. To verify that, male C57Bl/6 mice were subjected to 20% CR or ad libitum feeding, with variations in cage bedding and gut microbiota conditions. Additional groups received taurine supplementation or were fed a low-taurine diet (LTD). The results showed that in CR animals, taurine derived from the intestine was preferentially trafficked to epididymal white adipose tissue (eWAT) over other tested organs. Besides increased levels of taurine transporter TauT, gene expression of Cysteine dioxygenase (Cdo) involved in taurine synthesis was upregulated in CR eWAT. Taurine concentration in adipocytes was inversely correlated with fat pad weight of CR mice. Different types of cage bedding did not impact eWAT taurine levels; however, the lack of bedding and consumption of a diet high in soluble fiber did. Depleting gut microbiota with antibiotics or inhibiting bile salt hydrolase (BSH) activity reduced WAT taurine concentration in CR mice. Taurine supplementation increased taurine levels in WAT and brown adipose tissue (BAT), promoting fat loss in CR animals. LTD consumption blunted WAT loss in CR animals, with negligible impact on BAT. This study provides multiple insights into taurine's role in CR-triggered fat loss and describes a novel communication path between the liver, gut, microbiota, and WAT, with taurine acting as a messenger.
先前，我们已经证实，热量限制（CR）可刺激肠道中牛磺酸和胆汁酸的合成、共轭、分泌和去共轭，以及它们的再摄取。鉴于牛磺酸具有很强的抗肥胖特性，本研究旨在评估 CR 引起的牛磺酸动态平衡变化是否有助于脂肪组织损失。为了验证这一点，雄性 C57Bl/6 小鼠接受 20% CR 或自由喂养，同时改变笼子垫料和肠道微生物群条件。其他组接受牛磺酸补充或喂食低牛磺酸饮食（LTD）。结果表明，在 CR 动物中，来源于肠道的牛磺酸优先转运到附睾白色脂肪组织（eWAT），而不是其他测试器官。除了牛磺酸转运蛋白 TauT 的水平增加外，CR eWAT 中涉及牛磺酸合成的半胱氨酸双加氧酶（Cdo）基因表达也上调。脂肪细胞中的牛磺酸浓度与 CR 小鼠脂肪垫重量呈负相关。不同类型的笼子垫料不会影响 eWAT 中的牛磺酸水平；然而，缺乏垫料和摄入高可溶性纤维的饮食会影响。用抗生素耗尽肠道微生物群或抑制胆盐水解酶（BSH）活性会降低 CR 小鼠的 WAT 牛磺酸浓度。牛磺酸补充剂增加了 WAT 和棕色脂肪组织（BAT）中的牛磺酸水平，促进了 CR 动物的脂肪损失。LTD 消耗会减轻 CR 动物的 WAT 损失，但对 BAT 的影响可以忽略不计。本研究为牛磺酸在 CR 触发的脂肪损失中的作用提供了多个见解，并描述了肝脏、肠道、微生物群和 WAT 之间的一种新的通讯途径，牛磺酸作为一种信使。
