Abstract
Dept. of Endocrinology and Metabolism, University Hospital Maastricht, The Netherlands. wor@sint.azm.nl
BACKGROUND: Macrovascular disease is the leading cause of death in diabetes. The increased risk of atherosclerosis in diabetes may be partly explained by increased lipid peroxidation. METHODS: We assessed lipid peroxidation in subjects with type 2 diabetes with (n = 23) and without (n = 23) macrovascular complications versus healthy age-matched controls (n = 13). The diabetic groups were matched for glycemic control (mean HbA1c = 9%), and for age had similar known duration of diabetes. RESULTS: Plasma TBARS were comparable between diabetic subjects with and without macrovascular complications (1.89 +/- 0.32 and 1.81 +/- 0.28 mumol/l) and elevated compared to healthy controls (1.64 +/- 0.26 mumol/l, p = 0.025). Ratios of IgG and IgM antibodies to oxidized vs. native LDL were comparable between diabetic subjects and controls, and also between diabetic subjects with or without macrovascular complications. The lag phase, an index of the resistance of LDL to oxidation, was significantly longer in diabetic patients with macrovascular complications (66 +/- 8 min) vs. those without macrovascular complications and controls (resp. 59 +/- 7 and 56 +/- 7 min, p < 0.05). An explanation may be the frequent use of drugs with possible antioxidant potential, e.g. beta-blocking agents, ACE-inhibitors and calcium entry blockers by these patients. Surprisingly, plasma vitamin E levels were higher in diabetic subjects. CONCLUSIONS: We found no evidence of increased lipid peroxidation in diabetic subjects with macrovascular complications, but an increased resistance to oxidation in this group, probably due to an altered antioxidant status. The increased TBARS level in diabetic subjects contrasts with the other indices of lipid peroxidation and may be related to prevalent hyperglycemia and should therefore be interpreted cautiously.
Publication Types:
Clinical Trial
Controlled Clinical Trial
BACKGROUND: Macrovascular disease is the leading cause of death in diabetes. The increased risk of atherosclerosis in diabetes may be partly explained by increased lipid peroxidation. METHODS: We assessed lipid peroxidation in subjects with type 2 diabetes with (n = 23) and without (n = 23) macrovascular complications versus healthy age-matched controls (n = 13). The diabetic groups were matched for glycemic control (mean HbA1c = 9%), and for age had similar known duration of diabetes. RESULTS: Plasma TBARS were comparable between diabetic subjects with and without macrovascular complications (1.89 +/- 0.32 and 1.81 +/- 0.28 mumol/l) and elevated compared to healthy controls (1.64 +/- 0.26 mumol/l, p = 0.025). Ratios of IgG and IgM antibodies to oxidized vs. native LDL were comparable between diabetic subjects and controls, and also between diabetic subjects with or without macrovascular complications. The lag phase, an index of the resistance of LDL to oxidation, was significantly longer in diabetic patients with macrovascular complications (66 +/- 8 min) vs. those without macrovascular complications and controls (resp. 59 +/- 7 and 56 +/- 7 min, p < 0.05). An explanation may be the frequent use of drugs with possible antioxidant potential, e.g. beta-blocking agents, ACE-inhibitors and calcium entry blockers by these patients. Surprisingly, plasma vitamin E levels were higher in diabetic subjects. CONCLUSIONS: We found no evidence of increased lipid peroxidation in diabetic subjects with macrovascular complications, but an increased resistance to oxidation in this group, probably due to an altered antioxidant status. The increased TBARS level in diabetic subjects contrasts with the other indices of lipid peroxidation and may be related to prevalent hyperglycemia and should therefore be interpreted cautiously.
Publication Types:
Clinical Trial
Controlled Clinical Trial
| Original language | English |
|---|---|
| Pages (from-to) | 61-68 |
| Number of pages | 8 |
| Journal | Netherlands Journal of Medicine |
| Volume | 53 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 1 Jan 1998 |