Elevated Levels of Mannose-Binding Lectin (MBL) in patients with Type 2 Diabetes and its Potential Association with Nephropathy and Retinopathy

The hepatic protein Mannose-binding lectin (MBL) serves a pivotal role in the acute-phase immune response, potentially influencing the pathogenesis of type 2 diabetes (T2DM) and its associated complications, such as nephropathy and retinopathy. Recent evidence suggests that elevated plasma MBL levels may serve as a predictive marker for albuminuria in T2DM patients. Moreover, it is postulated that MBL ligands are present within the kidneys of diabetic individuals, thereby facilitating the deposition of MBL within the renal parenchyma or other target organs, thereby exacerbating pathological processes. This study aimed to assess serum MBL levels in T2DM patients and explore potential associations between MBL levels and the onset of diabetic complications. A cross-sectional investigation was conducted, encompassing 92 participants, comprising 71 individuals diagnosed with T2DM and 21 age- and sex-matched healthy counterparts. Among the T2DM cohort, patients were stratified into nephropathic and non-nephropathic subgroups based on the presence of nephropathy, as well as into subgroups with or without retinopathy based on retinopathy status. Serum MBL levels were quantified utilizing Enzyme-Linked Immunosorbent Assay (ELISA). The mean MBL levels were found to be significantly elevated in diabetic patients compared to healthy controls (1736 vs. 730.99 ng/mL, p-value = 0.011). Furthermore, MBL levels exhibited a statistically significant increase in individuals with microalbuminuria compared to normoalbuminuric T2DM patients (p-value = 0.019). Notably, a significant association was observed between heightened MBL levels in diabetic patients and the occurrence of retinopathy. The findings of this study support the hypothesis implicating MBL in the pathogenesis of T2DM and the initiation and progression of its associated complications, including nephropathy and retinopathy. Nevertheless, further investigation is warranted to delineate the precise underlying mechanisms governing the relationship between MBL and T2DM pathophysiology.