Inflammation in Type 2 diabetes mellitus and its complications

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, β-cell dysfunction, and persistent hyperglycemia. Growing evidence indicates that chronic low-grade inflammation plays a central role in the development and progression of T2DM and its associated complications. This review examines the inflammatory mechanisms underlying T2DM, focusing on cytokine signaling, immune cell activation, and inflammasome pathways that contribute to metabolic dysfunction. Obesity-associated adipose tissue inflammation promotes the release of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), which disrupt insulin signaling and impair glucose homeostasis. Activation of the NLRP3 inflammasome further amplifies inflammatory responses, leading to β-cell dysfunction and reduced insulin secretion. Inflammatory processes also contribute to the development of major diabetic complications, including diabetic nephropathy, retinopathy, neuropathy, and atherosclerotic cardiovascular disease. Elevated inflammatory biomarkers such as C-reactive protein (CRP), TNF-α, and IL-6 are consistently associated with disease progression and increased cardiovascular risk. While current pharmacological treatments primarily focus on glycemic control, increasing attention has been directed toward therapies that target inflammatory pathways. Anti-inflammatory strategies, including cytokine inhibition and inflammasome modulation, have shown potential in improving metabolic outcomes and reducing cardiovascular risk. Targeting inflammation therefore represents a promising complementary approach in the management of T2DM and its complications.