间歇性禁食会增加脂肪氧化,并促进瘦小鼠的代谢灵活性,但不是肥胖的2型糖尿病小鼠
Meghan O Conn1,2,3, Daniel M Marko1,2,3, Jonathan D Schertzer1,2,3
1Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
American journal of physiology. Endocrinology and metabolism
|August 28, 2024
概括
间歇性禁食在瘦小鼠中增强了代谢灵活性和脂质氧化,但在肥胖和2型糖尿病的小鼠中并非如此. 这表明代谢疾病会损害身体在禁食期间适应基质利用的能力.
科学领域:
- 代谢生理学 代谢生理学
- 内分泌学 在内分泌学.
- 营养科学 营养科学
背景情况:
- 肥胖和2型糖尿病 (T2D) 与代谢不灵活性有关,影响基质利用.
- 间歇性禁食 (IF) 显示出改善代谢灵活性的潜力.
- 在肥胖和T2D的背景下,IF对代谢灵活性的影响仍然不清楚.
研究的目的:
- 研究重复间歇性禁食如何影响2型糖尿病肥胖小鼠的代谢灵活性 (db/db),与瘦肉对照 (db/+) 相比.
- 为了确定IF是否可以提高脂肪酸氧化和代谢灵活性,而不依赖于体重变化.
主要方法:
- 肥胖 (db/db) 和瘦 (db/+) 的雄性小鼠接受了5:2间歇性禁食方案 (24小时快速,每周两次,持续10周).
- 评估的体重,组成,食物摄入量,身体活动,基质氧化 (脂肪酸和碳水化合物),血清β-基酸和脂肪细胞大小.
- 通过在IF后的食和禁食状态下测量基质氧化来评估代谢灵活性.
主要成果:
- 在任何一组中,IF疗法都没有改变身体质量,组成,食物摄入量或活动.
- 瘦小鼠在IF后表现出脂肪酸氧化和代谢灵活性增加,而肥胖小鼠表现出脂质代谢受损和持续的代谢不灵活性.
- 肥胖小鼠在IF后的瘦小鼠相比,血清β-基酸盐的含量较低,脂肪细胞大小没有变化.
结论:
- 重复间歇性禁食促进了新陈代谢的灵活性,并增加了脂肪酸氧化在瘦小鼠没有减肥.
- 肥胖和2型糖尿病显著损害了对间歇性禁食的适应性反应,防止了代谢灵活性和脂质氧化的改善.
- 这些发现强调,与肥胖和T2D相关的代谢功能障碍限制了间歇性禁食对基质代谢的益处.
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