小柯机器人

新加坡国立大学医学院Lei Sun和美国哥伦比亚大学Li Qiang研究团队合作取得一项新成果。经过不懈努力，他们的研究发现衰老和肥胖个体的代谢弹性下降。相关论文于2023年8月24日发表于国际学术期刊《细胞-代谢》杂志。

研究人员将适应和恢复营养波动的能力称为“代谢弹性”，并通过随意禁食-再喂养周期对其进行建模。代谢弹性通过协调各种基因表达来实现，研究人员将其称之为“基因弹性”。研究人员研发了一种系统的基因弹性评分方法，用于量化小鼠和非人灵长类动物中转录组在代谢活跃组织中的弹性。参与脂质和碳水化合物代谢的基因表现出较高的基因弹性，其弹性随着年龄的增长而下降，特别是在脂肪组织PPARγ失调时。

研究人员通过定时喂养激动剂使PPARγ活性与营养条件同步实现了其代谢益处和安全性的优化。研究进一步扩大了与饮食相关代谢和基因弹性的概念范围，揭示了饮食引起的肥胖与衰老之间存在相似的弹性下降。总之，该研究结果为揭示衰老和肥胖患者的代谢异常提供了见解。

据悉，生物体必须适应营养供应波动以维持能量稳态。

附：英文原文

Title: Deciphering the decline of metabolic elasticity in aging and obesity

Author: Qiuzhong Zhou, Lexiang Yu, Joshua R. Cook, Li Qiang, Lei Sun

Issue&Volume: 2023-08-24

Abstract: Organisms must adapt to fluctuating nutrient availability to maintain energy homeostasis.Here, we term the capacity for such adaptation and restoration “metabolic elasticity”and model it through ad libitum-fasting-refeeding cycles. Metabolic elasticity is achieved by coordinate versatilityin gene expression, which we call “gene elasticity.” We have developed the gene elasticityscore as a systematic method to quantify the elasticity of the transcriptome acrossmetabolically active tissues in mice and non-human primates. Genes involved in lipidand carbohydrate metabolism show high gene elasticity, and their elasticity declineswith age, particularly with PPARγ dysregulation in adipose tissue. Synchronizing PPARγactivity with nutrient conditions through feeding-timed agonism optimizes their metabolicbenefits and safety. We further broaden the conceptual scope of metabolic and geneelasticity to dietary challenges, revealing declines in diet-induced obesity similarto those in aging. Altogether, our findings provide a dynamic perspective on the dysmetabolicconsequences of aging and obesity.

DOI: 10.1016/j.cmet.2023.08.001

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00296-6

Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
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