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代谢性酸中毒和肾脏疾病如何加速衰老进程。

How metabolic acidosis and kidney disease may accelerate the aging process.

作者信息

Frassetto Lynda Ann, Sebastian Anthony, DuBose Thomas Durward

机构信息

University of California San Francisco, San Francisco, CA, USA.

Wake Forest School of Medicine, Winston-Salem, NC, USA.

出版信息

Eur J Clin Nutr. 2020 Aug;74(Suppl 1):27-32. doi: 10.1038/s41430-020-0693-5.

Abstract

Consuming a lower acid (and particularly lower phosphate) diet and/or supplementing the diet with base precursors, such as bicarbonate, might have a number of mitigating effects on the aging process. These include: (1) slowing progression of fibrosis by reduction of high endogenous acid production to preserve net acid excretion and minimize the degree of systemic acidosis; (2) avoiding the downregulation of klotho, a membrane and soluble factor associated with aging. Klotho declines when constant high dietary phosphate intake leads to an increase in FGF23 production; and (3) increasing activity of the enzyme telomerase, an important factor in maintaining telomere length, another factor associated with longer lifespan. Current evidence is based on studies in invertebrate and small animal models. These results, and extrapolations of associated human studies, suggest that low acid-producing diets, or neutralization of the low grade metabolic acidosis seen in humans with age-related renal dysfunction could potentially lead to a longer, healthier lifespan.

摘要

食用低酸(尤其是低磷)饮食和/或用碱前体(如碳酸氢盐)补充饮食,可能对衰老过程有多种缓解作用。这些作用包括:(1)通过减少内源性高酸产生来减缓纤维化进程,以维持净酸排泄并最小化全身酸中毒程度;(2)避免与衰老相关的膜结合和可溶性因子——klotho的下调。当持续高磷饮食摄入导致成纤维细胞生长因子23(FGF23)产生增加时,klotho会下降;以及(3)增加端粒酶的活性,端粒酶是维持端粒长度的重要因素,而端粒长度与更长的寿命相关。目前的证据基于对无脊椎动物和小动物模型的研究。这些结果以及相关人体研究的推断表明,低酸产生的饮食,或中和人类因年龄相关肾功能障碍而出现的轻度代谢性酸中毒,可能潜在地导致更长、更健康的寿命。

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