Food allergies are increasingly prevalent worldwide, yet the underlying immunometabolic mechanisms remain incompletely elucidated. Lactylation, as an emerging post-translational modification, has recently been identified as a critical regulator of immunometabolic reprogramming and inflammatory responses in allergic diseases. This review synthesizes current evidence on the role of lactylation in modulating immune cell dynamics, including macrophage polarization, dendritic cell antigen presentation, T-cell differentiation, mast cell activation, and neutrophil function. By systematically integrating lactate metabolism with lactylation-mediated epigenetic regulation, this review highlights their central role in shaping allergic inflammation, thereby linking metabolism to immune regulation in food allergies. Despite the research progress, challenges remain in understanding the transient nature of lactylation and tissue-specific dynamics. Future research should combine spatial omics, lactylation-specific imaging, and physiologically relevant models to clarify its spatiotemporal regulation. Meanwhile, dietary strategies, microbiota-based interventions, and pharmacological regulation may provide practical approaches for modulating lactate metabolism and lactylation.

Type 2 diabetes is a metabolic disease characterized by chronic hyperglycemia and relative insulin deficiency. As the disease progresses, type 2 diabetes often develop pathological changes in the liver such as inflammatory edema, fatty degeneration and liver fibrosis, which can develop into cirrhosis and, in severe cases, even liver cancer. Ginsenosides, the major bioactive components of the ginseng plant, show significant pharmacological effects on alleviating type 2 diabetic blood glucose disorders and liver damage. Their mechanism of action is mainly by regulating liver glucose and lipid metabolism, improving insulin sensitivity, and reducing hepatocyte apoptosis through the alleviation oxidative stress and the inhibition of inflammatory responses, thereby effectively alleviating liver damage and promoting liver function recovery. This article provides a systematic review of the effects and mechanisms of ginsenosides on alleviating diabetic liver injury and briefly outlines the pathogenesis of type 2 diabetic liver lesions, with the aim to provide a theoretical basis and practical reference for further investigating the hypoglycemic mechanism of ginsenosides and developing hypoglycemic and hepatoprotective drugs.

Natural compounds, including polysaccharides, alkaloids and polyphenols, have been shown to regulate immune responses within the tumor microenvironment (TME). These compounds achieve this by activating immune cells, inhibiting tumor cell proliferation, and promoting apoptosis. Furthermore, they modulate both immunosuppressive and immunoactivated states in the TME by influencing the activity of mast cells (MCs). MCs, as early and persistent infiltrating cells, play a pivotal role in allergic diseases and participate in various physiological and pathological processes. Their functions are primarily mediated through angiogenesis, tissue remodeling, and immunomodulation within the immune microenvironment. However, the role of MCs in tumorigenesis remains controversial. Depending on the tumor type, MCs exhibit remarkable plasticity and secrete a diverse array of signaling molecules that can significantly influence tumor progression. This review seeks to offer new insights into the role of MCs in tumorigenesis and development. Additionally, it explores the impact of natural compounds on the TME through MCs, contributing to a more comprehensive understanding of cancer therapy. Ultimately, this research aims to provide a scientific foundation for the development of novel tumor treatment strategies and to advance cancer therapy.