Relationship between metabolic glycaemic control and platelet content of glutathione and its related enzymes, in insulin-dependent diabetes mellitus

The relationship between glycaemic metabolic control and intracellular conc entration of reduced glutathione (GSH) and related enzymes GSH-peroxidase ( GSH-Px), GSH-reductase (GSH-Red), GSH-transferase (GSH-Tr), glucose-6-P-deh ydrogenase (G6PDH), and thioltransferase (TT) in patients with insulin-depe ndent diabetes mellitus (IDDM) is controversial. Choosing platelets as cell model (as commonly done in previous studies), the aim of this study was to relate the platelet content of GSH and related enzymes to glycaemic metabo lic control, expressed as glycated haemoglobin (HbA1c), as well as to prese nce of retinopathy and nephropathy in 114 IDDM patients. As compared to con trols, both GSH and GSH-Red (geometric means (95% CI)) were significantly i ncreased in platelets of diabetic patients: 3.3 (0.7-9.6) vs. 2.4 (0.8-7.6) mmol 10(-9) platelets; P = 0.01 for GSH, and 30.6 (14.7-61.6) vs. 22.2 (8. 7-52.2) mU 10(-9) platelets, P = 0.0002 for GSH-Red, and TT activity was ma rginally decreased in the IDDM group (P = 0.06), While no clear relationshi p was present between GSH-related enzymes and HbA1c, a trend was present to ward a non-linear relation between HbA1c and GSH, being significantly relat ed by a parabolic curve (P = 0.002). As compared to patients with normoalbu minuria (n = 88), diabetic patients with increased urinary albumin excretio n rate (n = 26) had a significant decrease in platelet TT concentration (3. 2 (0.9-6.7) vs, 5.1 (1.9-18.7) mU 10(-9) platelets; P = 0.0002), whereas re tinopathy was not associated to modifications in GSH or in the enzymatic pa ttern. In summary: (a) platelet GSH and GSH-Red are increased in IDDM. whil e other enzymes are unmodified: (b) GSH seems to be related to metabolic co ntrol according lu non-linear parabolic curve: (c) presence of increased al buminuria is associated to a selective decrease in platelet TT content. (C) 2000 Elsevier Science B.V. All rights reserved.