KIU Publications

Anaemia is a frequent but often under-recognized complication of type 2 diabetes mellitus (T2DM). Traditionally, anaemia in diabetes has been attributed mainly to diabetic kidney disease and reduced erythropoietin production. However, growing evidence shows that anaemia in T2DM is also strongly influenced by immunometabolic dysfunction, where chronic metabolic stress, inflammation, oxidative injury, mitochondrial dysfunction, iron restriction, and impaired erythropoiesis interact. T2DM is characterized by insulin resistance, hyperglycaemia, lipotoxicity, adipose tissue inflammation, endothelial dysfunction, and immune-cell reprogramming. These changes activate innate and adaptive immune pathways, leading to increased production of inflammatory mediators such as interleukin-6, tumour necrosis factor-alpha, interleukin-1β, and C-reactive protein. Inflammation alters iron metabolism through the hepcidin–ferroportin axis, causing functional iron deficiency and reduced haemoglobin synthesis. At the same time, oxidative stress and mitochondrial dysfunction impair haematopoietic stem cells, erythroid progenitor maturation, red blood cell survival, and bone marrow microenvironment function. Diabetic kidney disease further contributes through tubulointerstitial injury, reduced erythropoietin synthesis, and hypoxia-signalling defects. This review examines the immunometabolic mechanisms linking T2DM to anaemia, highlighting inflammation, iron dysregulation, renal impairment, erythropoietic stress, mitochondrial damage, and therapeutic implications.