Endocrine-Immune Mechanisms Linking Obesity, Diabetes, and Anaemia of Chronic Disease
Kungu Erisa
Faculty of Pharmacy Kampala International University Uganda
Email: erisa.kungu@studwc.kiu.ac.ug
ABSTRACT
Obesity, type 2 diabetes mellitus, and anaemia of chronic disease are increasingly recognized as interconnected disorders driven by persistent endocrine-immune dysregulation. Obesity is not merely excess fat accumulation but a chronic inflammatory and hormonal state characterized by adipocyte hypertrophy, adipose tissue hypoxia, macrophage infiltration, insulin resistance, altered adipokine secretion, oxidative stress, and low-grade systemic inflammation. These changes promote the development of type 2 diabetes by impairing insulin signalling in adipose tissue, skeletal muscle, liver, pancreatic β-cells, vascular endothelium, and immune cells. At the same time, chronic inflammation alters iron metabolism and erythropoiesis, creating the biological basis for anaemia of chronic disease. Central to this process is the hepcidin-ferroportin axis. Inflammatory cytokines, particularly interleukin-6, stimulate hepatic hepcidin production, leading to ferroportin degradation, iron sequestration within macrophages, reduced intestinal iron absorption, and restricted iron delivery to the bone marrow. In diabetes, this inflammatory iron restriction is compounded by kidney disease, reduced erythropoietin production, oxidative injury, mitochondrial dysfunction, nutritional deficiencies, and shortened red blood cell survival. This review examines the endocrine-immune mechanisms linking obesity, diabetes, and anaemia of chronic disease, with emphasis on adipokines, cytokines, insulin resistance, hepcidin, erythropoietin impairment, and therapeutic implications.
Keywords: Obesity; type 2 diabetes mellitus; anaemia of chronic disease; hepcidin; immunometabolism
CITE AS: Kungu Erisa (2026). Endocrine-Immune Mechanisms Linking Obesity, Diabetes, and Anaemia of Chronic Disease. IDOSR JOURNAL OF APPLIED SCIENCES 11(2):1-7. https://doi.org/10.59298/IDOSRJAS/2026/1121700