Authors: H A Jamieson V C Cogger S M Twigg S V McLennan A Warren R Cheluvappa S N Hilmer R Fraser R de Cabo D G Le Couteur
Publish Date: 2007/06/29
Volume: 50, Issue: 9, Pages: 1969-1976
Abstract
Diabetes mellitus is associated with extensive vascular pathology yet little is known about its longterm effects on liver sinusoidal endothelial cells LSECs Potential diabetic changes in LSECs are important because of the role played by fenestrations in the LSECs in hepatic disposition of lipoproteinsThere was an increase in the thickness of LSECs 170 ± 17 vs 123 ± 10 nm p 001 Fenestrations in LSECs as determined by overall porosity were markedly reduced 14 ± 01 vs 26 ± 02 p 001 Increased numbers of stellate cells were seen on electron microscopy and this finding was corroborated by increased smooth muscle actin expression Diabetes mellitus was also associated with increased endothelial production of von Willebrand factor and caveolin1Diabetes mellitus in the nonhuman primate is associated with marked changes in LSECs including a reduction in fenestrations Such changes provide an additional and novel mechanism for impaired hepatic lipoprotein clearance and postprandial hyperlipidaemia in diabetes mellitusThe vascular complications of diabetes mellitus are well established and have major clinical significance 1 However little is known about the effects of diabetes mellitus on the hepatic microvascular system The hepatic microvasculature consists of sinusoids which are porous gossamerlike vessels that connect afferent portal triads to exiting central hepatic venules over a distance of about 1 mm Approximately one billion sinusoids form the rich capillary network of the liver which permits the vast hepatic blood flow to course slowly and intimately between the cords of hepatocytes 2 3
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