与饮食诱导的肝脂肪减少相关的脂质组变化 青少年男孩与代谢功能障碍相关的脂肪性肝病
Helaina E Huneault1, Chih-Yu Chen2, Catherine C Cohen3
1Nutrition & Health Sciences Doctoral Program, Laney Graduate School, Emory University, Atlanta, GA 30322, USA.
低自由糖饮食 (LFSD) 通过减少有害脂质,如甘油三和胆固醇等,改善了青少年男孩的代谢功能障碍相关的脂肪性肝病 (MASLD). 这表明饮食可以使脂质代谢正常化并减少肝脏脂肪.
科学领域:
- 代谢障碍 代谢障碍 代谢障碍
- 营养科学 营养科学
- 利皮多米克 (Lipidomics) 是一种消化剂.
背景情况:
- 代谢功能障碍相关的脂肪性肝病 (MASLD) 在青少年中很常见,但其回归期间的脂质变化不明.
- 之前的研究表明,低自由糖饮食 (LFSD) 在患有MASLD的青少年中改善了肝肥胖症和de novo脂质生成 (DNL).
研究的目的:
- 为了研究LFSD干预后患有肝硬化症的青少年男孩的脂质适应.
- 为了确定与MASLD回归相关的饮食变化影响的特定脂质物种和途径.
主要方法:
- 在青少年男孩的样本上使用非向性和向性脂类药物 (LC-MS/MS),随机分为LFSD或常规饮食.
- 分析了甘油三 (TGs),二甲酸甘油 (DGs),胆固醇 (ChE),酸盐胆 (LPC),酸盐胆 (PC) 和氧利平的变化.
- 利用网络分析来检查富含棕酸盐的TG物种.
主要成果:
- 与对照组相比,LFSD组显示TG,DG,ChE,LPC和PC物种的显著减少.
- 在干预后,富含棕酸盐的TG物种显著下降,与减少的DNL相关.
- 氧化平素分析显示,8-异质和14,15-二甲降低,8,9-二甲增加,表明氧化应激改善.
结论:
- 与MASLD进展相关的LFSD正常化关键脂类物种 (TG,DG,ChE,PC,LPC) 的饮食干预.
- 研究结果表明,LFSD改善了患有MASLD的青少年的脂质代谢,胰岛素抵抗和脂毒性.
- 观察到的eicosanoids的变化表明氧化应激的潜在改善,需要进一步研究作为生物标志物.
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