Nutrient Metabolism & Signalling Laboratory, Department of Biochemistry and Molecular Biology, Metabolism, Diabetes and Obesity Program, Biomedicine Discovery Institute, Monash University, 3800 Clayton, Australia.
Division Chronic Inflammation and Cancer, German Cancer Research Center, 69120 Heidelberg, Germany.
Nutrients. 2021 Apr 26;13(5):1469. doi: 10.3390/nu13051469.
Prior studies have reported that dietary protein dilution (DPD) or amino acid dilution promotes heightened water intake (i.e., hyperdipsia) however, the exact dietary requirements and the mechanism responsible for this effect are still unknown. Here, we show that dietary amino acid (AA) restriction is sufficient and required to drive hyperdipsia during DPD. Our studies demonstrate that particularly dietary essential AA (EAA) restriction, but not non-EAA, is responsible for the hyperdipsic effect of total dietary AA restriction (DAR). Additionally, by using diets with varying amounts of individual EAA under constant total AA supply, we demonstrate that restriction of threonine (Thr) or tryptophan (Trp) is mandatory and sufficient for the effects of DAR on hyperdipsia and that liver-derived fibroblast growth factor 21 (FGF21) is required for this hyperdipsic effect. Strikingly, artificially introducing Thr de novo biosynthesis in hepatocytes reversed hyperdipsia during DAR. In summary, our results show that the DPD effects on hyperdipsia are induced by the deprivation of Thr and Trp, and in turn, via liver/hepatocyte-derived FGF21.
先前的研究报告表明,饮食蛋白质稀释(DPD)或氨基酸稀释会促进饮水量增加(即多饮),然而,确切的饮食需求和导致这种效果的机制仍不清楚。在这里,我们表明,饮食氨基酸(AA)限制足以并需要在 DPD 期间驱动多饮。我们的研究表明,特别是饮食必需氨基酸(EAA)限制,而不是非 EAA,是总饮食 AA 限制(DAR)引起多饮的原因。此外,通过使用不同量的个体 EAA 的饮食在恒定的总 AA 供应下,我们证明限制苏氨酸(Thr)或色氨酸(Trp)是必需的和足以影响 DAR 对多饮的作用,并且肝源性成纤维细胞生长因子 21(FGF21)是这种多饮作用所必需的。引人注目的是,在肝细胞中人为引入 Thr 从头合成逆转了 DAR 期间的多饮。总之,我们的结果表明,DPD 对多饮的影响是由 Thr 和 Trp 的剥夺引起的,进而通过肝/肝细胞衍生的 FGF21 引起的。