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Narative Review Volume 13 Issue 1
Pathological lipid redistribution as a shared immunometabolic axis in chronic communicable and non-communicable diseases
Mosab Nouraldein Mohammed Hamad
Received: January 29, 2026 | Published: February 16, 2026
Citation: Hamad MNM. Pathological lipid redistribution as a shared immunometabolic axis in chronic communicable and non-communicable diseases. J Diabetes Metab Disord Control. 2026;13(1):14-16. DOI: 10.15406/jdmdc.2026.13.00306
Abstract
Chronic diseases, encompassing both communicable and non-communicable conditions, are increasingly recognized as disorders of persistent immune and metabolic dysregulation rather than isolated pathological events. Excessive dietary fat intake has long been associated with inflammation and metabolic dysfunction. However, emerging evidence suggests that lipid distribution and cellular handling of lipids are critical determinants of disease persistence. Glycerolipids and triglycerides play central roles in immunometabolism, macrophage polarization, microbial survival, and pain modulation. Macrophages exhibit pronounced metabolic plasticity in response to lipid availability, and dysregulated lipid handling promotes dominance of alternatively activated (M2) macrophages. Although M2 macrophages contribute to inflammation resolution and tissue repair, sustained M2 polarization is associated with impaired microbial clearance, immune tolerance, fibrosis, and chronic disease progression. Pathogens such as Mycobacterium tuberculosis exploit host lipid stores to support long-term persistence, while chronic metabolic disorders exhibit abnormal lipid compartmentalization across circulation, tissues, and immune cells. Concurrently, alterations in glycerolipid and triglyceride profiles influence nociceptor activity and pain signaling, further linking lipid metabolism to clinical disease manifestations. Here, we hypothesize that pathological redistribution and dysregulated handling of glycerolipids and triglycerides—rather than their absolute abundance— constitute a shared immunometabolic axis that promotes M2 macrophage dominance, impairs microbial clearance, alters pain signaling, and contributes to the persistence of both communicable and non-communicable chronic diseases. This conceptual framework integrates metabolic disease, chronic infection, immune tolerance, and pain biology into a unified model. If validated, this hypothesis would shift current paradigms toward therapeutic strategies aimed at restoring physiological lipid distribution and macrophage metabolic balance, offering novel opportunities for intervention across a broad spectrum of chronic diseases.
Keywords: Immunometabolism, lipid redistribution, glycerolipids, triglycerides, M2 macrophages, chronic inflammation, metabolic–immune crosstalk, pain modulation
©2026 Hamad. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.