Are Lipoprotein(a) levels decreased in insulin resistance and type 2 diabetes?

Purpose of review Lipoprotein(a) [Lp(a)] is a significant player in cardiovascular disease (CVD) and type 2 diabetes (T2D). While Lp(a) contributes to residual cardiovascular risk in T2D, lower levels paradoxically increase the risk of developing T2D. This review explores Lp(a)'s dual role in cardiometabolic disease, its association with T2D, and emerging Lp(a)–lowering therapies Recent findings Large-scale studies confirm Lp(a) as a potent risk factor for cardiovascular events in T2D, with lower Lp(a) thresholds increasing risk compared to nondiabetic individuals. Observational and genetic studies reveal an inverse relationship between Lp(a) and T2D risk, linked to insulin dynamics, Kringle IV-type-2 repeat variants, and metabolic pathways. Emerging evidence suggests a connection between Lp(a), nonalcoholic fatty liver disease, and statin use. However, Mendelian randomization analyses have yielded conflicting results, leaving key mechanistic questions unresolved Summary Lp(a) plays a complex role in cardiometabolic health, acting as both a cardiovascular hazard and a potential metabolic marker in T2D. The paradoxical association of low Lp(a) with increased T2D risk challenges conventional perspectives and raises concerns regarding Lp(a)-lowering interventions. Further research is needed to clarify causality, refine risk stratification, and guide clinical decisions for Lp(a) modulation in T2D patients.