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Volume 52, Issue 12, Pages 1576-1578 (December 2003)


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Effect of improving glycemic control on low-density lipoprotein particle size in type 2 diabetes

Ana Marı́a Wägnera, Oscar Jorbaa, Mercedes Riglaa, Rosa Bonetb, Alberto de Leivaa, Jordi Ordóñez-Llanosbc, Antonio PérezCorresponding Author Informationa

Received 13 February 2003; accepted 9 June 2003.

Abstract 

The current study sought to assess the effect of improving glycemic control in type 2 diabetes on the components of diabetic dyslipidemia, especially low-denisty lipoprotein (LDL) size. A total of 33 type 2 diabetic patients (48.5% women, age 59.6 ± 11.1 years, body mass index [BMI] 28.9 ± 4.9, diabetes duration 6 [0 to 40] years, 40.7% on insulin) were seen at the hospital because of poor glycemic control (hemoglobin A1c [HbA1c] 10.33% ± 1.89%). Triglyceride, LDL-cholesterol (LDLc, Friedewald/ ultracentrifugation), high-density lipoprotein HDL-cholesterol (HDLc, direct method), apolipoproteins AI (apoAI) and B (apoB) (immunoturbidimetry), and LDL size (gradient gel electrophoresis) were measured at baseline and after improvement in glycemic control (decrease ≥ 1 percentage point in HbA1c and final HbA1c ≤ 8%). Improvement in glycemic control (HbA1c 7.01% ± 0.63%, P < .0005 v baseline) after a follow-up of 3.5 (range, 1 to 13) months resulted in a significant reduction in LDLc (3.34 ± 1.02 v 3.62 ± 1.15 mmol/L, P < .05) and apoB (1.07 ± 0.25 v 1.17 ± 0.29 g/L, P < .01) and an increase in HDLc (1.21 ± 0.32 v 1.13 ± 0.34 mmol/L, P < .05) and apoAI (1.36 ± 0.24 v 1.27 ± 0.24 mmol/L, P < 0.01) in the whole group, and an increase in LDL particle size (25.61 ± 0.53 v 25.10 ± 0.31 nm, P < .005) in the 14 patients showing LDL phenotype B at baseline. No significant changes were seen in body weight or BMI. We conclude that improvement of glycemic control in type 2 diabetes improves most of the components of diabetic dyslipidemia, including a shift towards larger LDL particles in subjects with phenotype B.

a Department of Endocrinology, Hospital Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain

b Department of Biochemistry, Hospital Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain

c Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, Barcelona, Spain

Corresponding Author InformationAddress reprint requests to Antonio Pérez, MD, PhD, Endocrinology and Nutrition Department, Hospital de Sant Pau, S Antonio M Claret 167, 08025 Barcelona, Spain

PII: S0026-0495(03)00326-3

doi:10.1016/S0026-0495(03)00326-3


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