美国威尔康奈尔医学院David E. Cohen课题组研究发现，微生物组缺陷型小鼠在葡萄糖稳态中适应性产热消失。这一研究成果于2020年2月20日发表在《细胞—代谢》杂志上。
为了测试这一点，他们在两种互补的肠道微生物缺陷小鼠模型中评估了能量消耗和葡萄糖代谢，给这些模型施加广泛的热应激和饮食压力。肠道微生物组的清除或寒冷环境温度引起的大量微生物干扰，都不会影响小鼠接触冷或高脂喂养期间的能量消耗。
尽管如此，他们证明了肠道微生物代谢在通过产生氨基酸代谢物来维持血糖正常中的关键作用，这些氨基酸代谢物优化了肝TCA（三羧酸）循环通量以支持糖异生。这些结果区别了肠道微生物组在调节能量消耗方面的可分配性及其对维持葡萄糖稳态的关键作用。
据介绍，最近的研究表明，肠道微生物组影响能量平衡和葡萄糖稳态的关键机制是通过募集棕色和米色的脂肪细胞，它们是适应性产热反应的主要介质。
附：英文原文
Title: Dissociation of Adaptive Thermogenesis from Glucose Homeostasis in Microbiome-Deficient Mice
Author: Tibor I. Krisko, Hayley T. Nicholls, Curtis J. Bare, Corey D. Holman, Gregory G. Putzel, Robert S. Jansen, Natalie Sun, Kyu Y. Rhee, Alexander S. Banks, David E. Cohen
Issue&Volume: 2020-02-20
Abstract: Recent studies suggest that a key mechanism whereby the gut microbiome influencesenergy balance and glucose homeostasis is through the recruitment of brown and beigeadipocytes, primary mediators of the adaptive thermogenic response. To test this,we assessed energy expenditure and glucose metabolism in two complementary mouse modelsof gut microbial deficiency, which were exposed to a broad range of thermal and dietarystresses. Neither ablation of the gut microbiome, nor the substantial microbial perturbationsinduced by cold ambient temperatures, influenced energy expenditure during cold exposureor high-fat feeding. Nevertheless, we demonstrated a critical role for gut microbialmetabolism in maintaining euglycemia through the production of amino acid metabolitesthat optimized hepatic TCA (tricarboxylic acid) cycle fluxes in support of gluconeogenesis.These results distinguish the dispensability of the gut microbiome for the regulationof energy expenditure from its critical contribution to the maintenance of glucosehomeostasis.
DOI: 10.1016/j.cmet.2020.01.012
Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30013-9
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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本期文章：《细胞—代谢》：Online/在线发表
