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Diabetes, Vol 46, Issue 7 1207-1213, Copyright © 1997 by American Diabetes Association
Optimization of glycemic control by insulin therapy decreases the proportion of small dense LDL particles in diabetic patients
A Caixas, J Ordonez-Llanos, A de Leiva, A Payes, R Homs and A Perez
Endocrinology Department, Hospital de Sant Pau, Universitat Autnoma de Barcelona, Spain.
Small dense LDL particles (B phenotype) are considered to be more
atherogenic than large buoyant LDL particles. The influence of glycemic
control on LDL particle size and density is still under debate. The aim of
this study was to determine LDL subfraction phenotype in both IDDM and
NIDDM patients in poor glycemic control compared with that of respective
matched control groups. In addition, we evaluated the effect of a 3-month
period of optimized glycemic control on this parameter. Thirty-seven IDDM
patients and 33 NIDDM patients, together with two respective age-, sex-,
and BMI-matched control groups were studied. Non-A phenotype prevalence in
IDDM patients before (19%) and after blood glucose optimization (11%) was
similar to that of their control group (12%). However, NIDDM patients
displayed a higher proportion of the non-A phenotype (51%) than did the
control group (28%), but it became closer (30%, P < 0.05) after glycemic
control improved. All subjects with non-A phenotype that changed to A
phenotype showed triglyceride levels below 1.63 mmol/l and a greater
decrease in HbA1c than did subjects whose phenotype did not change (4.9 +/-
1.5 vs. 3.1 +/- 1.4%, P < 0.05). A higher proportion of small dense LDL
was observed in NIDDM women than in nondiabetic women (LDL5 10.0 +/- 4.8
vs. 6.3 +/- 1.5%, LDL6 6.1 +/- 2.2 vs. 4.2 +/- 0.8%, P < 0.05) during
both stages of glycemic control, but no differences were observed between
NIDDM and nondiabetic men. In conclusion, these findings provide new
evidence for the relevance of near-normal glycemic control in the
prevention of macrovascular disease and could contribute to an explanation
of the loss of protection for cardiovascular disease in diabetic women.

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Copyright © 1997 by the American Diabetes Association.
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