日本庆应义塾大学医学院Kenya Honda团队的一项最新研究提出了微生物介导的米色脂肪细胞对饮食线索的反应。这一研究成果于2026年3月4日发表在国际顶尖学术期刊《自然》上。

在这里，研究团队表明蛋白质的可用性深刻地调节肠道微生物群的功能景观，并促进白色脂肪组织（WAT）的重塑。具体来说，低蛋白饮食（LPDs）可以明显诱导WAT中褐变的特征基因，其程度与经典刺激（如冷暴露或β-肾上腺素能受体激活）的反应相似。在无菌小鼠中，LPD介导的褐变明显减少，这种缺陷是通过用由从LPD喂养的小鼠或健康人类志愿者的粪便中分离和筛选的菌株组成的特定细菌群定植而挽救的，这些菌株具有18F氟脱氧葡萄糖正电子发射断层扫描（FDG-PET）证实的棕色或米色脂肪活性。

微生物诱导的褐变是由胆汁酸介导的，胆汁酸驱动脂肪祖细胞中farnesoid X受体（FXR）的激活，nrfa编码的评论衍生氨驱动成纤维细胞生长因子的表达。FGF21在肝细胞中的表达。胆汁酸-FXR轴和氨-FGF21轴在促进WAT褐变过程中都具有非冗余的重要作用。这些发现强调了饮食、肠道微生物代谢和脂肪组织重塑之间的机制联系，揭示了宿主对饮食线索作出反应的微生物依赖途径。

研究人员表示，饮食和肠道菌群之间的相互作用是代谢健康、形成能量平衡和疾病易感性的基础。然而，饮食和微生物因素共同调节宿主生理的潜在机制尚不清楚。

附：英文原文

Title: Microbiota-mediated induction of beige adipocytes in response to dietary cues

Author: Tanoue, Takeshi, Nagayama, Manabu, Roochana, Ayumi J. A., Zimmerman, Samuel, Ashenberg, Orr, Jain, Tanvi, Igarashi, Ryo, Sasajima, Satoshi, Takeshita, Kozue, Hetherington, Nicola, Okahashi, Nobuyuki, Ueda, Masahiro, Konishi, Morichika, Nakayama, Yoshiaki, Minoda, Aki, Skelly, Ashwin N., Minokoshi, Yasuhiko, Pucci, Nicholas, Mende, Daniel R., Arita, Makoto, Yamamoto, Hironori, Watanabe, Shunji, Miura, Kouichi, Behie, Scott W., Suda, Wataru, Sato, Toshiro, Atarashi, Koji, Matsushita, Mami, Kajimura, Shingo, Plichta, Damian R., Saito, Masayuki, Xavier, Ramnik J., Honda, Kenya, Tanoue, Takeshi, Nagayama, Manabu, Roochana, Ayumi J. A., Zimmerman, Samuel, Ashenberg, Orr, Jain, Tanvi, Igarashi, Ryo, Sasajima, Satoshi, Takeshita, Kozue, Hetherington, Nicola, Okahashi, Nobuyuki, Ueda, Masahiro, Konishi, Morichika, Nakayama, Yoshiaki, Minoda, Aki, Skelly, Ashwin N., Minokoshi, Yasuhiko, Pucci, Nicholas, Mende, Daniel R., Arita, Makoto, Yamamoto, Hironori, Watanabe, Shunji, Miura, Kouichi, Behie, Scott W., Suda, Wataru, Sato, Toshiro, Atarashi, Koji

Issue&Volume: 2026-03-04

Abstract: Interactions between diet and the gut microbiota are fundamental to metabolic health, shaping energy balance and disease susceptibility1,2,3,4,5. However, the underlying mechanisms by which dietary and microbial factors converge to regulate host physiology remain unclear. Here we show that protein availability profoundly modulates the functional landscape of the gut microbiota and promotes remodelling of white adipose tissue (WAT). Specifically, low-protein diets (LPDs) robustly induce signature genes of browning in WAT to a similar extent to that seen in response to classical stimuli, such as cold exposure or β-adrenergic receptor activation6,7,8. LPD-mediated browning was markedly diminished in germ-free mice, and this defect was rescued by colonization with defined bacterial consortia made up of strains that were isolated and down-selected from the faeces of either LPD-fed mice or healthy human volunteers with 18F-fluorodeoxyglucose positron emission tomography (FDG-PET)-confirmed brown- or beige-fat activity9,10,11,12. Microbiota-induced browning was mediated both by bile acids driving the activation of the farnesoid X receptor (FXR) in adipose progenitor cells, and by nrfA-encoding commensal-derived ammonia driving the expression of fibroblast growth factor21 (FGF21) in hepatocytes. The bile acid–FXR and ammonia–FGF21 axes both have non-redundant, essential roles in promoting WAT browning. These findings highlight a mechanistic link between diet, gut microbial metabolism and adipose tissue remodelling, uncovering microbiota-dependent pathways by which the host responds to dietary cues.

DOI: 10.1038/s41586-026-10205-3

Source: https://www.nature.com/articles/s41586-026-10205-3