Chronic Inflammation in Diabetes: Mechanisms Linking Hyperglycaemia to Immune Dysregulation

Ivan Mutebi

Department of Pharmacognosy Kampala International University Uganda

Email: ivan.mutebi@studwc.kiu.ac.ug

                                                                        ABSTRACT
Chronic inflammation is a hallmark of diabetes mellitus and a key driver of its long-term complications. Hyperglycaemia triggers a cascade of molecular and cellular events that disrupt immune homeostasis, promote persistent low-grade inflammation, and impair resolution pathways. This review synthesizes current understanding of the mechanisms linking elevated glucose levels to immune dysregulation, including advanced glycation end product (AGE) formation, oxidative stress, metabolic reprogramming of immune cells, inflammasome activation, and dysregulated cytokine networks. We discuss how these processes converge to sustain chronic inflammation, contribute to insulin resistance, endothelial dysfunction, and tissue damage in organs such as the vasculature, kidneys, liver, nerves, and retina. We also examine emerging biomarkers of inflammatory activity in diabetes and evaluate therapeutic strategies targeting inflammatory pathways, including glycaemic control, anti-inflammatory agents, immune modulators, and lifestyle interventions. A clearer understanding of how hyperglycaemia orchestrates immune dysfunction will enhance prevention and treatment of diabetic complications and inform precision medicine approaches.

Keywords: chronic inflammation, diabetes mellitus, hyperglycaemia, immune dysregulation, advanced glycation end products.

CITE AS: Ivan Mutebi (2026). Chronic Inflammation in Diabetes: Mechanisms Linking Hyperglycaemia to Immune Dysregulation. NEWPORT INTERNATIONAL JOURNAL OF BIOLOGICAL AND APPLIED SCIENCES 7(2):15-22. https://doi.org/10.59298/NIJBAS/2026/7.2.1522