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5-Heptadecylresorcinol通过调节脂肪Sirtuin 3来改善与衰老相关的肝脂肪酸氧化功能障碍

Kuiliang Zhang¹, Lei Jiang¹, Lamei Xue¹

¹State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

|April 13, 2024

概括

5-Heptadecylresorcinol (AR-C17) 改善了老年小鼠与衰老相关的脂肪酸氧化功能障碍. 这种化合物通过调节白色脂肪组织中的Sirt3来增强热生成和新陈代谢,间接有利于肝功能.

科学领域:

代谢健康和衰老研究
营养科学和功能性食品

背景情况:

衰老会损害肝脂肪酸 (FA) 的氧化,影响适应性热生成.
在全麦和麦中发现的5-Heptadecylresorcinol (AR-C17),通过调节Sirt3.3,显示了改善老年小鼠热生成的潜力.
AR-C17对与衰老相关的肝脏FA氧化功能障碍的特定影响尚未完全理解.

研究的目的:

为了研究AR-C17对与衰老相关的肝脏FA氧化功能障碍的影响.
阐明AR-C17影响肝脏FA氧化的机制,特别是它与白色脂肪组织 (WAT) 中的Sirt3的关系.

主要方法:

在18个月大的C57BL/6J小鼠口服AR-C17 (150毫克/公斤/天,持续8周) 时.
评估全身葡萄糖和脂质代谢,肝脏FA氧化和WAT脂解.
使用脂肪特异性的Sirt3淘汰赛小鼠来验证调节途径.

主要成果:

在老年小鼠中,AR-C17的使用改善了肝脏FA的氧化和甲酸代谢,特别是在冷刺激期间.
在AR-C17治疗后,观察到全身葡萄糖和脂质代谢的增强.
AR-C17改善了WAT脂解,并促进了肝脏的乙卡尼丁生产.
在脂肪特异性Sirt3淘汰赛小鼠中,AR-C17对WAT脂解和肝脏FA氧化的有益影响被废除了.

结论:

AR-C17改善了与衰老相关的肝脏FA氧化功能障碍.
该机制涉及AR-C17通过调节白色脂肪组织中的Sirt3来间接影响肝脏FA氧化.

关键词:

5-heptadecylresorcinol的使用情况.脂肪 Sirt3 脂肪 Sirt3 脂肪老化的老化衰老的老化脂肪酸氧化过程中的脂肪酸氧化.肝脏肝脏肝脏肝脏肝脏肝脏

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