Table 4. Effects of intensive insulin treatment on systemic oxidative stress and glutathione synthesis.
CIT | IIT | p | ||
---|---|---|---|---|
Treatment effects | Treatment × protocol interaction | |||
Plasma TBARS (nmol×mL-1) |
2.9±0.4 | 2.2±0.2 | 0.04 | 0.54 |
Erythrocyte glutathione FSR (%×day) |
43±11 | 97±29 | 0.02 | 0.11 |
Erythrocyte glutathione ASR (mmol× L(HCT)-1×day-1) | 1.18±0.29 | 2.70±0.51 | 0.01 | 0.12 |
Erythrocyte glutathione ASR (mmol×g(Hb)-1×day-1) | 0.03±0.008 | 0.08±0.018 | 0.009 | 0.09 |
Erythrocyte GCL-C (fraction of GAPDH) |
0.73±0.08 | 0.83±0.22 | 0.61 | 0.42 |
IIT, Intensive insulin therapy; CIT, Conventional insulin therapy; HCT, hematocrit; Hb, hemoglobin, TBARS, thiobarbituric acid reactive substances; FSR, fractional synthesis rate; ASR, absolute synthesis rate; GCL-C, glutamate cysteine ligase–catalytic subunit; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. Data are means±SEM of pooled values from protocols 1 and 2 obtained at the end of CIT and IIT periods. Data were analyzed with repeated measures ANOVA, with treatment as within subjects variables (control and intensive insulin treatment) and sequence of treatments as between subjects factor [protocol 1 (n = 5), IIT first, CIT second; protocol 2 (n = 5), CIT first, IIT second].