Diabetes mellitus is a multifaceted metabolic disorder characterized by chronic hyperglycemia, arising from defects in insulin secretion, insulin action, or both. Beyond its well-documented metabolic underpinnings, emerging evidence has illuminated a pivotal role of inflammation in the pathogenesis of diabetes. Pro-inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β), disrupt insulin signaling, impair β-cell function, and exacerbate insulin resistance. Chronic low-grade inflammation serves as a unifying mechanism linking obesity, metabolic dysfunction, and diabetes progression. The interplay between inflammatory pathways and diabetes extends to both type 1 and type 2 diabetes. In type 1 diabetes, autoimmune-mediated β-cell destruction is driven by inflammatory cytokines and dysregulated immune responses, while in type 2 diabetes, systemic and adipose tissue inflammation perpetuate insulin resistance and β-cell stress. Key molecular players, including toll-like receptors, the NLRP3 inflammasome, and the c-Jun N-terminal kinase (JNK) pathway, act as mediators between metabolic stress and inflammatory responses, emphasizing the bidirectional relationship between inflammation and hyperglycemia.
Emmanuel Ifeanyi Obeagu (Fri,) studied this question.