Immunometabolic Remodeling in Diabetes: Impacts on Organ Toxicity and Disease Progression
Kungu Erisa
Faculty of Pharmacy Kampala International University Uganda
Email: erisa.kungu@studwc.kiu.ac.ug
ABSTRACT
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia and disturbances in carbohydrate, lipid, and protein metabolism. Beyond classical metabolic derangements, diabetes induces profound immunometabolic remodeling that reshapes cellular energy utilization, immune functions, and tissue homeostasis. This remodeling plays a central role in the initiation and progression of diabetic complications, including cardiovascular disease, nephropathy, neuropathy, retinopathy, and nonalcoholic fatty liver disease (NAFLD). Immunometabolic changes involve chronic low-grade inflammation, immune cell dysregulation, increased production of reactive oxygen species (ROS), and alterations in nutrient-sensing pathways such as AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB). These pathways intersect with metabolic signaling to drive organ-specific toxicity and accelerate disease progression. This comprehensive review synthesizes current knowledge on immunometabolic interactions in diabetes, highlights mechanisms linking metabolic dysfunction and immune responses, and discusses the impact of immunometabolic remodeling on organ damage. We also evaluate emerging biomarkers and therapeutic strategies that modulate immunometabolic pathways to prevent or attenuate diabetic complications. A deeper understanding of immunometabolic remodeling offers new avenues for precision medicine in diabetes management.
Keywords: Immunometabolism, diabetes complications, inflammation, metabolic signaling, organ toxicity.
CITE AS: Kungu Erisa (2026). Immunometabolic Remodeling in Diabetes: Impacts on Organ Toxicity and Disease Progression. NEWPORT INTERNATIONAL JOURNAL OF BIOLOGICAL AND APPLIED SCIENCES 7(2):7-14. https://doi.org/10.59298/NIJBAS/2026/7.2.714