ISSN:
1432-0428
Keywords:
Lipoproteins
;
Type 1 (insulin-dependent) diabetes
;
blood glucose control
;
lipoprotein composition
;
atherosclerosis
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Plasma lipoprotein compositional abnormalities were investigated in eight normolipidaemic (plasma cholesterol 〈5.70 mmol/l; triglyceride 〈2.03 mmol/l) young male Type 1 (insulin-dependent) diabetic patients (before and after a short period of optimised blood glucose control) and in nine healthy control subjects, matched for sex, age and body mass index. Free and esterified cholesterol, triglyceride, phospholipids were assayed in all lipoprotein classes (VLDL, IDL, LDL) and in HDL subclasses (HDL2 and HDL3); apoB was measured only in very low density lipoproteins (VLDL). All VLDL constituents were increased in the diabetic group, the differences being more striking for apoB (6.0±1.1 mg/dl vs 2.0±0.1 mg/dl, p〈0.02), free cholesterol (0.27±0.04 mmol/l vs 0.13±0.02 mmol/l, p〈0.02) and esterified cholesterol (0.32±0.08 mmol/l vs 0.13±0.01 mmol/l, p〈0.05). Also HDL subfractions showed differences between the two groups: all HDL2 constituents were increased, while in HDL3 only triglyceride was significantly increased (0.11±0.01 mmol/l vs 0.08±0.004 mmol/l, p〈0.02). After two weeks of optimised blood glucose control all VLDL constituents were reduced and particularly: esterified cholesterol (−39%, p〈0.02), free cholesterol (−37%, p〈0.05), apoB (− 35%, p〈0.05). Expressing each VLDL constituent as percent of the total lipoprotein mass, it was evident that the diabetic VLDL was rich in cholesterol both esterified (8.4±1.0% vs 5.4±0.5%, p〈0.02) and free (8.5±0.7% vs 5.5±0.3%, p〈0.001), apo B (5.1±0.6% vs 2.6±0.3%, p〈0.001) and depleted in triglyceride (57.0±1.7% vs 64.1±1.7%, p〈0.001). Two weeks of optimised blood glucose control were not able to correct the abnormal composition of VLDL. In conclusion, Type 1 (insulin-dependent) diabetic patients, although normolipidaemic, show an abnormal VLDL composition suggesting an increased prevalence of smaller and, possibly, more atherogenic VLDL particles. This abnormality is not corrected by a short period of blood glucose optimisation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00265371
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