Erythrocyte fragility is amplified by oxidative stress and linked to diabetes-specific microvascular disease. Vitamin C supplementation improves glycemic indices in adults with type 2 diabetes (T2D) by improving antioxidant status. This cross-sectional study examined the relationships between vitamin C status and erythrocyte osmotic fragility in adults with or without T2D. Participants provided a fasting blood sample for erythrocyte osmotic fragility testing as a function of hypotonic NaCl concentrations. Additionally, plasma was stabilized with metaphosphoric acid prior to vitamin C analysis using isocratic reverse-phase UV-HPLC separation. Participants were grouped as diagnosed T2D (n = 14; 36% female; 55.5 ± 8.2 y; 31.5 ± 9.0 kg/m2; HbA1c: 7.4 ± 1.9%; plasma vitamin C: 36.0 ± 12.2 μM) or no diabetes (n = 16; 69% female; 38.7 ± 13.5 y; 26.8 ± 6.6 kg/m2; HbA1c: 5.4 ± 0.3%; plasma vitamin C: 34.8 ± 10.9 μM). Participant characteristics differed between groups only for age and hemoglobin A1c (HbA1c; p < 0.05). All hemolysis parameters were in normal ranges for the participants with T2D, and no significant differences in hemolysis parameters were noted between those with or without T2D. However, among participants with T2D, the NaCl concentration eliciting 50% hemolysis was higher for those with low (<7%) vs. high (>7%) HbA1c values (p = 0.037) indicating a slightly higher erythrocyte fragility in the former group. Vitamin C status did not impact any of the hemolysis parameters in adults with or without T2D. Thus, erythrocyte fragility was not elevated in T2D, and vitamin C nutriture was not related to erythrocyte fragility in adults with well-controlled T2D.

Objectives Erythrocyte osmotic fragility is noted in Gulo−/− knockout mice unable to synthesize vitamin C, likely due to the decreased production of cytoskeletal β-spectrin, which affects cell deformability. Individuals with type 2 diabetes (T2D) commonly display marginal vitamin C nutriture, a consequence of reduced cellular uptake and recycling of dehydroascorbic acid. This cross-sectional study examined the relationships between vitamin C status and erythrocyte osmotic fragility in adults with or without T2D. Methods Participants did not report unresolved disease conditions or supplementation with vitamin C for the previous three months. T2D diagnosis occurred ≥1 year before study enrollment. Participants provided a fasting venous blood sample for erythrocyte osmotic fragility testing based on erythrocyte lysis with varying concentrations of sodium chloride. In addition, plasma was extracted and mixed with equal volume of 10% (w/v) metaphosphoric acid in 2 mmol/L disodium EDTA and centrifuged at 4°C. The supernatant was stored at −80°C until analysis using isocratic reverse-phase UV-HPLC separation. All participants provided written informed consent and the study was approved by the local Institutional Review Board. Results Participant characteristics did not differ significantly between groups with the exception of age (P < 0.01) and HbA1c (p = 0.002). Data are presented for adults with T2D (n = 14; 36% female; 55.5 ± 8.2 y; 31.5 ± 9.0 kg/m2; HbA1c: 7.4 ± 1.9%; plasma vitamin C: 36.0 ± 12.2 mM) and adults without T2D (n = 16; 69% female; 38.7 ± 13.5 y; 26.8 ± 6.6 kg/m2; A1c: 5.4 ± 0.3%; plasma vitamin C: 34.8 ± 10.9 mM). Compared to adults with T2D, erythrocyte osmotic fragility was significantly elevated in adults without T2D at 0.35% saline (+4.4%, p = 0.021). Vitamin C status did not impact erythrocyte osmotic fragility in adults with T2D; however, in adults without T2D, erythrocyte osmotic stability was linked to high vitamin C status at 0.35% saline (p = 0.054 unadjusted and p = 0.022 adjusted for age and gender). Conclusions In this small pilot trial, T2D was not related to increased erythrocyte osmotic fragility or marginal vitamin C status. However, vitamin C nutriture was directly linked to erythrocyte osmotic stability in adults without T2D. Funding Sources This research received no external funding.