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		| Title: | Effect of improving glycemic control on low-density lipoprotein particle size in type 2 diabetes | Authors: | Wägner, Ana María Jorba, Oscar Rigla, Mercedes Bonet, Rosa De Leiva, Alberto Ordóñez-Llanos, Jordi Pérez, Antonio | UNESCO Clasification: | 32 Ciencias médicas 3205 Medicina interna | Keywords: | Dyslipidemia Diabetes Metabolic syndrome Lipoprotein | Issue Date: | 2003 | Journal: | Metabolism: Clinical and Experimental | 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. | URI: | https://accedacris.ulpgc.es/handle/10553/52034 | ISSN: | 0026-0495 | DOI: | 10.1016/S0026-0495(03)00326-3 | Source: | Metabolism: Clinical and Experimental[ISSN 0026-0495],v. 52(12), p. 1576-1578 (Diciembre 2003) | 
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