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低血糖饮食改变脂质代谢以影响瘤生长
Evan C Lien1, Anna M Westermark1, Yin Zhang2,3
1Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
卡路里限制 (CR),但不是性饮食 (KD),通过改变脂质代谢和甲酸脱酶 (SCD) 活性来抑制瘤生长. 饮食中的脂肪成分会影响瘤对这些饮食的反应.
科学领域:
- 癌症学
- 代谢研究
- 癌症代谢
背景情况:
- 饮食干预会影响瘤微环境和癌细胞代谢.
- 卡路里限制 (CR) 和性饮食 (KD) 通过降低葡萄糖和胰岛素来抑制瘤进展.
- 然而,只有CR可证明抑制了小鼠的某些瘤异位移植,这表明了其他机制.
研究的目的:
- 研究CR和KD影响瘤生长的机制.
- 探索脂质代谢和醇-CoA脱酶 (SCD) 在调解饮食干预的抗瘤作用中的作用.
主要方法:
- 在CR和KD小鼠中的瘤全移植生长的比较.
- 血和瘤中的脂质水平分析.
- 在瘤中评估stearoyl-CoA脱酶 (SCD) 的活性.
- 操纵SCD表达和食脂肪组成.
主要成果:
- 与KD不同的是,CR降低了血和瘤脂质水平,损害了瘤的生长.
- 抑制瘤SCD活动,造成不良的不和和和脂肪酸比率.
- 通过强制性SCD表达或增加脂质可用性,可以诱导瘤对CR的耐药性.
- 癌症也会影响瘤的SCD活动,但增加的脂质可用性会维持脂肪酸平衡.
- 修改KD脂肪成分以增加和脂肪酸可以增强瘤生长抑制.
结论:
- 脂肪酸脱和可用性的饮食诱导的改变决定了瘤对低血糖饮食的反应.
- 通过SCD抑制,CR通过破坏脂质代谢来抑制瘤生长.
- KD对瘤生长的影响取决于其脂肪成分及其与SCD活性的相互作用.
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