Zhang Hui, Cao Wanxiu, Liu Fang, Gao Yuan, Chang Yaoguang, Xue Changhu, Tang Qingjuan
College of Food Science and Engineering Ocean University of China Qingdao China.
Laboratory of Marine Drugs and Biological Products Pilot National Laboratory for Marine Science and Technology Qingdao China.
Food Sci Nutr. 2021 Sep 28;9(11):6232-6244. doi: 10.1002/fsn3.2581. eCollection 2021 Nov.
Previous study has suggested the colonic nontoxicity and obesity inhibition of food-grade κ-carrageenan in obese mice. Further study using transcriptome is important to provide further understanding on the gene expressions of inflammation and obesity. Here, the obese mice without any treatment (HFD) or with 5% food-grade κ-carrageenan diet intervention (H5%) were used to perform colonic transcriptome sequencing. The results showed that genes involved in the inflammatory pathways or tight junction protein encoding were not significantly dysregulated by 5% carrageenan. However, the expression of lipid metabolism genes meaningfully changed as evidenced by the decreased gene levels of adipocytokines, lipogenesis, lipid absorption and transport, and the increased adipolysis and oxidation. In addition, the carrageenan metabolism experiments by toluidine blue (TB) staining of colon and high-performance size exclusion chromatography (HPSEC) of feces supernatant showed that the food-grade κ-carrageenan was not absorbed or significantly degraded in the digestive tract of obese mice. Hence, the fact that food-grade κ-carrageenan was not significantly metabolized by the organism and did not cause obvious dysregulation of colonic inflammatory genes provided evidences for its noncolonic toxicity in obese mice. An anti-obesity potential of food-grade κ-carrageenan was probably mediated by the regulation of lipids metabolism-related genes.
先前的研究表明，食品级κ-卡拉胶对肥胖小鼠具有结肠无毒性和抑制肥胖的作用。进一步利用转录组进行研究，对于深入了解炎症和肥胖相关的基因表达具有重要意义。在此，使用未经任何处理的肥胖小鼠（高脂饮食组）或接受5%食品级κ-卡拉胶饮食干预的肥胖小鼠（H5%组）进行结肠转录组测序。结果显示，5%卡拉胶并未使参与炎症途径或紧密连接蛋白编码的基因发生显著失调。然而，脂质代谢基因的表达发生了有意义的变化，表现为脂肪细胞因子、脂肪生成、脂质吸收和转运相关基因水平降低，而脂肪分解和氧化相关基因水平升高。此外，通过结肠甲苯胺蓝（TB）染色和粪便上清液的高效尺寸排阻色谱（HPSEC）进行的卡拉胶代谢实验表明，食品级κ-卡拉胶在肥胖小鼠的消化道中未被吸收或显著降解。因此，食品级κ-卡拉胶未被机体显著代谢且未导致结肠炎症基因明显失调，这为其在肥胖小鼠中的结肠无毒性提供了证据。食品级κ-卡拉胶的抗肥胖潜力可能是通过调节脂质代谢相关基因来介导的。
