Caspase-1 as a Biomarker of Metabolic and Inflammatory Toxicity in Type 2 Diabetes Mellitus

Background: Persistent hyperglycemia and lipid imbalance in diabetes contribute to both metabolic and inflammatory toxicity. Caspase-1, a central component of the inflammasome, mediates pyroptosis and the maturation of pro-inflammatory cytokines. Objective: This study evaluates Caspase-1 as a potential biomarker linking metabolic derangement and inflammatory toxicity in individuals with Type 2 Diabetes Mellitus (T2DM). Methods: The levels of Caspase-1, TNF-α, IL-1β, albumin, HbA1c, HOMA-IR, and TyG index were measured in diabetic and control subjects. Correlation analyses examined the relationships between Caspase-1 and indicators of glycemic control and inflammation. Results: Caspase-1 concentrations were significantly elevated in diabetic subjects compared to controls (p < 0.001). Caspase-1 correlated positively with HbA1c, HOMA-IR, TyG, IL-1β, and TNF-α, but inversely with albumin. These relationships suggest that poor metabolic control and inflammatory toxicity are closely linked via inflammasome activation. Conclusion: Elevated Caspase-1 levels reflect the combined burden of metabolic and inflammatory toxicity in T2DM. The enzyme may serve as an integrative biomarker for assessing systemic toxic stress arising from metabolic dysregulation and chronic inflammation.