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Increased fatty acids in Type 1 Diabetes disrupts C‐peptide’s transport and downstream effect

C‐peptide, a hormone that is co‐secreted from the pancreatic beta‐cell, has been shown to alleviate diabetic complications attributed to poor microvascular blood flow. In this mechanism, C‐peptide binds to the red blood cell (RBC), increasing adenosine triphosphate (ATP) release and subsequent nitric oxide (NO) release, a potent vasodilator. Prior research has indicated that C‐peptide must be complexed with zinc (Zn2+) and albumin to elicit this response. However, in type 1 diabetes (T1D), increased basal levels of fatty acids result in high concentrations of fatty acids bound to albumin. These increased concentrations of fatty acids seen in T1D may have implications in C‐peptide’s transport and therapeutic effect. Here, the binding of C‐peptide, Zn2+ and albumin are measured with increased levels of a myristic acid, a common fatty acid seen in vivo.3D‐printed technologies were employed to fabricate an ultrafiltration device to measure the association between C‐peptide, Zn2+ and albumin. C‐peptide derived ATP release from RBCs was quantified via chemiluminescence on a spectrophotometer. Results indicate that C‐peptide binding to albumin is disrupted when myristic acid is in solution (3.68 nM free, n=12). In addition, C‐peptide derived ATP release from RBCs is decreased as concentrations of myristic acid increased. These discoveries indicate disruptions in C‐peptide’s transport and effect with increased fatty acids. In addition, these findings open an unprecedented area of study regarding other modifications in the bloodstream of people with T1D that may disrupt C‐peptide transport and delivery.