巨噬细胞通过饮食调节的PDGFcc产生来控制能量存储，这一成果由美国斯隆凯特林研究所Frederic Geissmann课题组完成。相关论文于2021年7月2日发表于国际学术期刊《科学》。

研究人员在遗传筛选中确定了血小板衍生生长因子（PDGF）/血管内皮生长因子（VEGF）家族直系同源物Pvf3，它由巨噬细胞产生，这是果蝇幼虫脂肪体细胞脂质储存所必需的。遗传和药理学实验表明，由脂肪组织驻留巨噬细胞产生的小鼠Pvf3直系同源物PDGFcc以瘦素受体和C-C趋化因子受体2型非依赖的方式控制脂肪细胞中的脂质储存。

PDGFcc的产生受饮食调节，并以旁分泌方式控制新生和成年小鼠脂肪组织中的脂质储存。在PDGFcc阻断后的生物体水平上，多余的脂质被重定向到棕色脂肪中的产热作用。这些数据确定了一种巨噬细胞依赖性机制，有利于药物干预的设计，并控制后生动物的能量储存。

据悉，巨噬细胞调节能量储存的机制仍然知之甚少。 

附：英文原文

Title: Diet-regulated production of PDGFcc by macrophages controls energy storage

Author: Nehemiah Cox, Lucile Crozet, Inge R. Holtman, Pierre-Louis Loyher, Tomi Lazarov, Jessica B. White, Elvira Mass, E. Richard Stanley, Olivier Elemento, Christopher K. Glass, Frederic Geissmann

Issue&Volume: 2021/07/02

Abstract: The mechanisms by which macrophages regulate energy storage remain poorly understood. We identify in a genetic screen a platelet-derived growth factor (PDGF)/vascular endothelial growth factor (VEGF)–family ortholog, Pvf3, that is produced by macrophages and is required for lipid storage in fat-body cells of Drosophila larvae. Genetic and pharmacological experiments indicate that the mouse Pvf3 ortholog PDGFcc, produced by adipose tissue–resident macrophages, controls lipid storage in adipocytes in a leptin receptor– and C-C chemokine receptor type 2–independent manner. PDGFcc production is regulated by diet and acts in a paracrine manner to control lipid storage in adipose tissues of newborn and adult mice. At the organismal level upon PDGFcc blockade, excess lipids are redirected toward thermogenesis in brown fat. These data identify a macrophage-dependent mechanism, conducive to the design of pharmacological interventions, that controls energy storage in metazoans.

DOI: 10.1126/science.abe9383

Source: https://science.sciencemag.org/content/373/6550/eabe9383