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Accelerated cholesteryl ester transfer in patients with insulin‐dependent diabetes mellitus
Author(s) -
BAGDADE J. D.,
RITTER M. C.,
SUBBAIAH P. V.
Publication year - 1991
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1991.tb01805.x
Subject(s) - medicine , endocrinology , cholesterylester transfer protein , very low density lipoprotein , diabetes mellitus , cholesterol , lipoprotein , metabolic control analysis , chemistry
. Abnormalities in cholesteryl ester transfer (CET) may play a role in the development of diabetic arterial vascular complications. To assess this important step systematically in reverse cholesterol transport, we have studied 20 treated, clinically stable, normolipidaemic patients. Contrary to the impairment in CET described previously in NIDDM, the mass of CE transferred from HDL to VLDL+LDL was significantly greater in IDDM patients than in controls at 1,2, and 4 h ( P <0.001). When the d <1.063 plasma fractions from IDDM subjects were combined with controls d <1.063 fractions, an accelerated CET response was observed which was identical to that found in intact IDDM plasma. This finding, which indicates that this disturbance in CET was associated with the acceptor lipoproteins, was confirmed when we found that it was reproduced by the addition of IDDM VLDL and not LDL to control d >1.063 fractions. Changes observed in lipoprotein core lipid composition were consistent with accelerated CET occurring in IDDM in vivo : the TG/CE core lipid ratio was decreased in VLDL from six subjects (diabetic 9.5±0.8 vs control 12.9±3.4; P <0.1) and increased in their HDL (diabetic 0.55±0.11 vs control 0.42±0.04; P <0.025). No correlation was demonstrable between estimates of diabetic control (glycoalbumin, fasting glucose) and CET. These data indicate that CET may be abnormally increased in normolipidaemic IDDM patients. A defect of this type may be atherogenic because it increases the number of lipoprotein particles in plasma which resemble cholesteryl ester‐enriched chylomicron and VLDL remnants but whose normal receptor‐mediated catabolism may be altered.