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Impaired endothelium-dependent vasodilation in type 2 diabetes. Relation to LDL size, oxidized LDL, and antioxidants
S Mäkimattila1, M L Liu, J Vakkilainen
1Department of Medicine, Helsinki University Central Hospital, Finland.
Insights
Type 2 diabetes impairs endothelial function, linked to smaller LDL particle size and higher triglycerides. Lower LDL particle size significantly correlates with reduced vasodilation, indicating a key factor in diabetes-related vascular issues.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Metabolic Syndrome
Background:
- Endothelial dysfunction is a hallmark of type 2 diabetes.
- Identifying determinants of this dysfunction is crucial for managing cardiovascular risk.
Purpose of the Study:
- To investigate the relationship between cardiovascular risk markers and endothelial function in type 2 diabetes.
- To determine specific factors contributing to endothelial dysfunction in this population.
Main Methods:
- Compared blood flow responses to endothelium-dependent and -independent agents in 30 men with type 2 diabetes and 12 controls.
- Analyzed cardiovascular risk markers including lipid profiles and LDL oxidation.
- Assessed antioxidant capacity via total peroxyl radical-trapping capacities (TRAPs).
Main Results:
- Type 2 diabetic subjects showed significantly lower acetylcholine-induced vasodilation compared to controls.
- Elevated serum triglycerides and smaller LDL particle size were observed in diabetic patients.
- LDL particle size was significantly correlated with endothelium-dependent vasodilation and serum triglycerides.
Conclusions:
- Patients with type 2 diabetes exhibit impaired endothelium-dependent vasodilation.
- Smaller LDL particle size is a significant determinant of endothelial dysfunction in type 2 diabetes.
- Elevated triglycerides and reduced LDL size are key vascular risk factors in this cohort.
Objective:
To search for determinants of endothelial dysfunction in type 2 diabetes.
Research Design And Methods:
We performed a comprehensive analysis of cardiovascular risk markers and measured blood flow responses to endothelium-dependent (acetylcholine [ACh] and NG-monomethyl-L-arginine) and -independent (sodium nitroprusside [SNP]) vasoactive agents in 30 nonsmoking men with type 2 diabetes (age 51 +/- 1 years, BMI 27.8 +/- 0.4 kg/m2, HbA1c 7.4 +/- 0.3%) and 12 matched normal control men.
Results:
ACh-induced vasodilation was 37% lower in type 2 diabetic (6.1 +/- 0.5) than in normal subjects (9.7 +/- 1.5 ml.dl-1.min-1, P < 0.01), while flows during SNP were similar (9.1 +/- 0.6 vs. 9.9 +/- 1.3 ml.dl-1.min-1, NS). The ratio of endothelium-dependent vs. -independent flow (ACh:SNP ratio) was 31% lower in type 2 diabetic (0.70 +/- 0.05) than in normal subjects (1.10 +/- 0.18, P < 0.01). Total (2.2 +/- 0.4 vs. 1.3 +/- 0.2 mmol/l, P < 0.05), VLDL, and intermediate-density lipoprotein triglycerides were significantly higher, and the mean LDL particle diameter was significantly smaller in type 2 diabetic than in normal subjects. The lag times for LDL oxidation by Cu2+ in vitro were similar in patients with type 2 diabetes (183 +/- 7) and in normal subjects (183 +/- 9 min, NS). Measured and calculated (sum of concentration of individual antioxidants in serum) total peroxyl radical-trapping capacities (TRAPs) were comparable between the groups. In the patients with type 2 diabetes, LDL size was significantly correlated with endothelium-dependent vasodilation (r = 0.43, P < 0.05), serum triglycerides (r = -0.75, P < 0.001), and the lag time for LDL oxidation in vitro (r = 0.38, P < 0.05). HbA1c was inversely correlated with the lag time for LDL oxidation in vitro (r = -0.41, P < 0.05) and TRAP.
Conclusions:
In summary, patients with type 2 diabetes exhibited impaired endothelium-dependent vasodilation in vivo, elevated serum triglycerides, decreased LDL size, and normal antioxidant capacity. Of these parameters, LDL size was significantly correlated with endothelial function.