Journal of Advances in Physical Medicine & Rehabilitation

Abstract

Chronic hyperglycemia is a defining characteristic of diabetes mellitus, a prolonged metabolic disorder resulting from inadequate insulin production, diminished insulin efficacy, or a combination of these factors. Increasing data indicates that inflammation strongly influences the aetiology of both Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM). Interleukins are pivotal inflammatory mediators in the disease process due to their regulation of immune responses, inflammation, and cellular metabolism. The article discusses the influence of interleukins on the development and progression of diabetes mellitus. Pro-inflammatory interleukins, including IL-1β, IL-6, and IL-17, facilitate the autoimmune destruction of pancreatic β-cells in type 1 diabetes via the activation of inflammatory pathways, oxidative stress, and immunological dysregulation. Moreover, the functionality of regulatory T cells is compromised by IL-2 depletion, which exacerbates autoimmunity. Chronic low-grade inflammation that obstructs insulin signalling and β-cell functionality in type 2 diabetes is associated with obesity and insulin resistance, mediated by cytokines such as IL-1β, IL-6, and IL-18. Conversely, the anti-inflammatory properties of interleukin-10 (IL-10) positively influence by diminishing inflammatory responses and enhancing insulin sensitivity. The progression of diabetes complications such as nephropathy, retinopathy, and cardiovascular issues is influenced by interleukins. The finding of molecular connections between interleukins and diabetes has facilitated the development of prospective treatment targets, including cytokine inhibitors and immunomodulatory approaches. Interleukins are significant biomarkers and therapeutic agents in the progression and management of diabetes mellitus.