Nonlinear HbA1c thresholds reveal accelerated atherogenic remodeling and improved risk reclassification in type 2 diabetes

Dysglycemia, lipid metabolism, and cardiovascular disease (CVD) progression in type 2 diabetes (T2D) are closely interconnected, yet the non-linear lipid remodeling processes underlying atherogenic dyslipidemia remain insufficiently defined. This study aimed to identify HbA1c thresholds associated with accelerated lipid-driven atherogenesis, quantify the mediating role of the triglyceride-to-HDL cholesterol ratio (TG/HDL-C) -a surrogate of insulin-resistance-related lipid metabolism-and assess the incremental predictive value of the Atherogenic Index of Plasma (AIP) within the clinically ambiguous "glycemic gray zone. " A total of 271 adults with T2D not receiving lipid-lowering therapy were retrospectively grouped by HbA1c: good (NRI) tested the added predictive value of AIP over conventional lipid markers. All atherogenic indices worsened with deteriorating glycemia (p < 0. 001). Non-linear inflection points were observed at HbA1c 8. 0% for TG/HDL-C and 8. 5% for AIP (pₙon-linearity < 0. 01). TG/HDL-C mediated 56. 9% of the HbA1c effect on AIP, indicating its central role in linking hyperglycemia to lipid remodeling. Adding AIP improved cardiovascular risk reclassification, particularly in the 8. 0%-8. 5% transition range (categorical NRI = 0. 384; 95% CI: 0. 184-0. 584). These findings identify 8. 0%-8. 5% as a metabolically vulnerable HbA1c threshold marked by accelerated atherogenic dyslipidemia. AIP functions as a sensitive lipid-based marker for cardiometabolic risk detection within this gray zone, while TG/HDL-C acts as a key mechanistic mediator, supporting the integration of atherogenic lipid indices into individualized risk assessment and precision lipid management strategies in T2D.