<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Chylomicron metabolism is abnormal in diabetes and the chylomicron
particle may play a very important role in atherosclerosis.
The aim of this study was to examine the effect of diabetes
on the metabolism of chylomicrons in cholesterol-fed alloxan diabetic
and nondiabetic rabbits. Five diabetic rabbits and 5 control
rabbits were given [<sup>14</sup>C]linoleic acid and [<sup>3</sup>H]cholesterol by
gavage. Lymph was collected following cannulation of the lymph
duct and radiolabelled chylomicrons were isolated by ultracentrifugation.
The chylomicrons from each animal were injected into
paired control and diabetic recipients. Lymph apolipoprotein (apo)
B48, apo B100, and apo E were measured using sodium dodecyl
sulfate–polyacrylamide gradient gel electrophoresis. Mean blood
sugar of the diabetic donors and diabetic recipients were 19.7 ± 2.3
and 17.2 ± 3.2 mmol/L. Diabetic rabbits had significantly
raised plasma triglyceride (10.8 ± 13.9 versus 0.8 ± 0.5 mmol/L,
<italic>P</italic> &lt; 0.02). There was a large increase in apo B48 in lymph chylomicrons
in the diabetic donor animals (0.19 ± 0.10 versus 0.04 ± 0.02
mg/h, <italic>P</italic> &lt; 0.01) and apo B100 (0.22 ± 0.15 versus 0.07 ± 0.07 mg/h,
<italic>P</italic> &lt; 0.05) and a reduction in apo E on the lymph chylomicron
particle (0.27 ± 0.01 versus 0.62 ± 0.07 mg/mg apo B, <italic>P</italic> &lt; 0.001).
Diabetic recipients cleared both control and diabetic chylomicron
triglyceride significantly more slowly than control recipients
(<italic>P</italic> &lt; 0.05). Clearance of control chylomicron cholesterol was delayed
when injected into diabetic recipients compared to when these
chylomicrons were injected into control recipients (<italic>P</italic> &lt; 0.005).
Clearance of diabetic chylomicron cholesterol was significantly
slower when injected into control animals compared to control chylomicron injected into control animals (<italic>P</italic> &lt; 0.02). In this animal
model of atherosclerosis, we have demonstrated that diabetes
leads to the production of an increased number of lipid and apo
E–deficient chylomicron particles. Chylomicron particles from the
control animals were cleared more slowly by the diabetic recipient
(both triglyceride and cholesterol). The chylomicron particles
obtained from the diabetic animals were cleared even more slowly
when injected into the diabetic recipient. Although there was an initial
delay in clearance of chylomicron triglyceride from the diabetic
particle when injected into the control animals, the clearance over
the first 15 minutes was not significantly different when compared
to the control chylomicron injected into the control animal. On the
other hand, the cholesterol clearance was significantly delayed.
Thus, diabetes resulted in the production of an increased number of
lipid- and apo E–deficient chylomicron particles. These alterations
account, in part, for the delay in clearance of these particles.</p>
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Int J Exp Diabetes Res. 2002; 3(3):171-178