The metabolism of macro- and micronutrients is a complex and highly regulated biological process. An imbalance in the metabolites and their signaling networks can lead to nonresolving inflammation and consequently to the development of chronic inflammatory-associated diseases. Therefore, identifying the accumulated metabolites and altered pathways during inflammatory disorders would not only serve as “real-time” markers but also help in the development of nutritional therapeutics. In this review, we explore recent research that has delved into elucidating the effects of carbohydrate/calorie restriction, protein malnutrition, lipid emulsions and micronutrient deficiencies on metabolic health and inflammation. Moreover, we describe the integrated stress response in terms of amino acid starvation and lipemia and how this modulates new age diseases such as inflammatory bowel disease and atherosclerosis. Lastly, we explain the latest research on metaflammation and inflammaging. This review focuses on multiple signaling pathways, including, but not limited to, the FGF21–β-hydroxybutryate–NLRP3 axis, the GCN2-eIF2α-ATF4 pathway, the von Hippel-Lindau/hypoxia-inducible transcription factor pathway and the TMAO-PERK-FoxO1 axis. Additionally, throughout the review, we explain how the gut microbiota responds to altered nutrient status and also how antimicrobial peptides generated from nutrient-based signaling pathways can modulate the gut microbiota. Collectively, it must be emphasized that metabolic starvation and inflammation are strongly regulated by both environmental (i.e., nutrition, gut microbiome) and nonenvironmental (i.e., genetics) factors, which can influence the susceptibility to inflammatory disorders.

大量营养素和微量营养素的代谢是一个复杂且高度调控的生物过程。代谢物及其信号网络的不平衡可能导致无法解决的炎症，从而导致慢性炎症相关疾病的发展。因此，识别炎症性疾病期间累积的代谢物和改变的途径不仅可以作为“实时”标记，还有助于营养疗法的开发。在这篇综述中，我们探讨了最近的研究，这些研究深入阐明了碳水化合物/热量限制、蛋白质营养不良、脂肪乳剂和微量营养素缺乏对代谢健康和炎症的影响。此外，我们描述了氨基酸饥饿和脂血症方面的综合应激反应，以及它如何调节炎症性肠病和动脉粥样硬化等新时代疾病。最后，我们解释了有关代谢炎症和炎症的最新研究。本综述重点关注多种信号通路，包括但不限于 FGF21-β-羟基丁酸-NLRP3 轴、GCN2-eIF2α-ATF4 通路、von Hippel-Lindau/缺氧诱导转录因子通路和 TMAO-PERK -FoxO1 轴。此外，在整个综述中，我们解释了肠道微生物群如何响应营养状态的改变，以及基于营养的信号通路产生的抗菌肽如何调节肠道微生物群。总的来说，必须强调的是，代谢饥饿和炎症受到环境（即营养、肠道微生物组）和非环境（即遗传）因素的强烈调节，这可以影响对炎症性疾病的易感性。