小柯机器人

中南大学罗湘杭团队发现，骨髓免疫细胞应对波动的营养压力来限制体重反弹。相关论文于近日在线发表在《细胞—代谢》杂志上。

研究人员发现了一种干细胞样的CD7⁺单核细胞亚群，它们在节食引起的体重减轻的小鼠和人类骨髓（BM）中聚集。CD7⁺单核细胞的过继转移可抑制体重反弹，而CD7⁺单核细胞的诱导性消耗则会加速体重反弹。这些细胞通过表观遗传适应积累了新陈代谢记忆，优先迁移到皮下白色脂肪组织（WAT），并在那里分泌纤维蛋白原样蛋白2（FGL2），激活蛋白激酶A（PKA）信号通路，进而促进米色脂肪产热。然而，CD7⁺单核细胞在减肥后会逐渐进入静止状态，同时体重增加。

值得注意的是，服用FMS样酪氨酸激酶3配体（FLT3L）能显著恢复CD7⁺单核细胞的活力，从而改善体重快速反弹的情况。总之，这些研究结果发现了一种独特的骨髓源性代谢记忆免疫细胞群，可以作为防治肥胖症的靶标。

据介绍，减肥后体重反弹是治疗肥胖症的一大挑战。免疫细胞能适应波动的营养压力，但它们在调节体重反弹中的作用仍不清楚。

附：英文原文

Title: Bone marrow immune cells respond to fluctuating nutritional stress to constrain weight regain

Author: Hai-Yan Zhou, Xu Feng, Li-Wen Wang, Rui Zhou, Heng Sun, Xin Chen, Ren-Bin Lu, Yan Huang, Qi Guo, Xiang-Hang Luo

Issue&Volume:

Abstract: Weight regain after weight loss is a major challenge in the treatment of obesity.Immune cells adapt to fluctuating nutritional stress, but their roles in regulatingweight regain remain unclear. Here, we identify a stem cell-like CD7+ monocyte subpopulation accumulating in the bone marrow (BM) of mice and humans thatexperienced dieting-induced weight loss. Adoptive transfer of CD7+ monocytes suppresses weight regain, whereas inducible depletion of CD7+ monocytes accelerates it. These cells, accumulating metabolic memories via epigeneticadaptations, preferentially migrate to the subcutaneous white adipose tissue (WAT),where they secrete fibrinogen-like protein 2 (FGL2) to activate the protein kinaseA (PKA) signaling pathway and facilitate beige fat thermogenesis. Nevertheless, CD7+ monocytes gradually enter a quiescent state after weight loss, accompanied by increasedsusceptibility to weight regain. Notably, administration of FMS-like tyrosine kinase3 ligand (FLT3L) remarkably rejuvenates CD7+ monocytes, thus ameliorating rapid weight regain. Together, our findings identifya unique bone marrow-derived metabolic-memory immune cell population that could betargeted to combat obesity.

DOI: 10.1016/j.cmet.2023.08.009

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00304-2

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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