PDF(Pubmed)
Abstract：
Recent literature extensively investigates the crucial role of energy metabolism in determining the inflammatory response and polarization status of macrophages. This rapidly expanding area of research highlights the importance of understanding the link between energy metabolism and macrophage function. The metabolic pathways in macrophages are intricate and interdependent, and they can affect the polarization of macrophages. Previous studies suggested that glucose flux through cytosolic glycolysis is necessary to trigger pro-inflammatory phenotypes of macrophages, and fatty acid oxidation is crucial to support anti-inflammatory responses. However, recent studies demonstrated that this understanding is oversimplified and that the metabolic control of macrophage polarization is highly complex and not fully understood yet. How the metabolic flux through different metabolic pathways (glycolysis, glucose oxidation, fatty acid oxidation, ketone oxidation, and amino acid oxidation) is altered by obesity- and type 2 diabetes (T2D)-associated insulin resistance is also not fully defined. This mini-review focuses on the impact of insulin resistance in obesity and T2D on the metabolic flux through the main metabolic pathways in macrophages, which might be linked to changes in their inflammatory responses. We closely evaluated the experimental studies and methodologies used in the published research and highlighted priority research areas for future investigations.
摘要：
最近的文献广泛研究了能量代谢在决定巨噬细胞的炎症反应和极化状态中的关键作用。这一迅速扩大的研究领域突出了理解能量代谢和巨噬细胞功能之间联系的重要性。巨噬细胞的代谢途径错综复杂且相互依赖，它们可以影响巨噬细胞的极化。以前的研究表明，通过细胞溶质糖酵解的葡萄糖通量是触发巨噬细胞促炎表型所必需的，脂肪酸氧化对支持抗炎反应至关重要。然而,最近的研究表明，这种理解过于简单化，巨噬细胞极化的代谢控制非常复杂，尚未完全理解。代谢如何通过不同的代谢途径(糖酵解，葡萄糖氧化，脂肪酸氧化，酮氧化，和氨基酸氧化）因肥胖而改变，2型糖尿病（T2D）相关的胰岛素抵抗也未完全定义。这篇小型综述集中在肥胖和T2D对通过巨噬细胞主要代谢途径的代谢通量的影响。这可能与他们炎症反应的变化有关。我们密切评估了已发表研究中使用的实验研究和方法，并强调了未来研究的优先研究领域。
