脑卒中后白质损伤修复与感觉运动功能的恢复和认知功能障碍密切相关。忽略了白质损伤的保护和修复是绝大多数神经保护制剂在脑卒中临床转化中以失败告终的重要原因。小胶质细胞/巨噬细胞在脑卒中后的组织损伤与修复过程中发挥重要作用，“经典激活”M1型小胶质细胞释放促炎因子，加重白质损伤；“转化激活”M2小胶质细胞则有助于减轻白质损伤，促进白质修复。我们研究表明限食能够减轻成年小鼠脑缺血/再灌注引起的白质损伤，促进长期神经功能恢复，其白质保护作用与促进循环系统中脂联素的增加有关。我们发现脂联素受体1不仅表达于神经元、星形胶质细胞和小胶质细胞，而且在成熟少突胶质细胞也有表达，可能介导了限食的白质保护作用。因此，提出假设：限食可能通过激活小胶质细胞/巨噬细胞脂联素受体1促进其M2极化，或直接作用于少突胶质细胞及其前体细胞的脂联素受体1减轻白质损伤，促进白质结构和功能重塑，改善脑卒中后的长期神经功能。

White matter injury induced by ischemic stroke results in the long-term dysfunctions of sensorimotor activities and cognitive functions. Insufficient recovery of white matter after ischemic stroke attributes to the failure of therapeutic strategies in translational stroke research. Microglia/macrophages play a critical role in white matter injury and recovery process after cerebral ischemia. Classically polarized M1 microglia release destructive pro-inflammatory factors and exacerbate white matter injury, while alternative polarized M2 microglia could alleviate white matter injury and promote its recovery after cerebral ischemia. We have reported that calorie restriction could alleviate white matter injury and neurological deficits induced by cerebral ischemia in adult mice. Calorie restriction increased the adiponectin concentration in circulation, contributing to preserve white matter integrity. We for the first time demonstrated that adiponectin receptor 1 not only expressed in neurons, astrocytes and microglia, but also in mature oligodendrocytes and myelin structure, suggesting that adiponection receptor 1 may participate in calorie restriction-afforded white matter protection after cerebral ischemia. Thus, we hypothesized that calorie restriction could activate adiponectin receptor 1 on microglia/macrophages to facilitate its M2 polarization, and directly activate adiponectin receptor 1 on oligodendrocytes and its precursor cells to alleviate white matter injury and enhance the reconstruction white matter to improve neurological functions after ischemic stroke.