Tight Glycemic Control Regulates Fibronectin Expression and Basement Membrane Thickening in Retinal and Glomerular Capillaries of Diabetic Rats

2009 ◽  
Vol 50 (2) ◽  
pp. 943 ◽  
Author(s):  
Saira Cherian ◽  
Sumon Roy ◽  
Andre Pinheiro ◽  
Sayon Roy
2000 ◽  
Vol 1 (1) ◽  
pp. 19-30 ◽  
Author(s):  
Michele Doucet ◽  
Irene Londoño ◽  
Amparo Gómez-Pascual ◽  
Moise Bendayan

In diabetes, the glomerular basement membrane undergoes thickening and structural alterations with loss of glomerular permselectivity properties. However, the onset of the alterations at early phases of diabetes is unclear. Aiming to determine the functional and structural alterations of the glomerular wall in the early stages of diabetes, we have studied the distribution of endogenous circulating albumin and type IV collagen in the glomerular basement membrane, using the immunocytochemical approach. The streptozotocin-injected hyperglycemic rat was our animal model. Renal tissues were examined after 10 days, 2, 4 and 6 months of hyperglycemia. Upon immunogold labelings, changes in the glomerular permeability to endogenous albumin were found altered as early as upon ten days of hyperglycemia. In contrast, no structural modifications were detected at this time point. Indeed, glomerular basement membrane thickening and an altered type IV collagen labeling distribution were only observed after four months of hyperglycemia, suggesting that functional alterations take place early in diabetes prior to any structural modification. In order to evaluate the reversibility of the glomerular alterations, two-month-old diabetic animals were treated with insulin. These animals showed a significant restoring of their glomerular permselectivity. Our results suggest a link between glycemic levels and alteration of glomerular permeability in early stages of diabetes, probably through high levels of glycated serum proteins.


Author(s):  
Timothy J. Benstead ◽  
Virgilio E. Sangalang

AbstractBackgroundDespite the potential importance of endoneurial microvessel abnormalities in diabetic neuropathy, the pathogenesis of these abnormalities is incompletely understood. We wished to evaluate the effect of experimental diabetes on endoneurial microvessels and determine if an aldose reductase inhibitor alters any of the changes induced by diabetes.MethodsWe compared streptozocin diabetic rats with and without aldose reductase inhibitor treatment to non-diabetic rats after 10 months of diabetes. Transverse microvessels from the mid-sciatic level were studied by electron microscopic morphometric evaluation.ResultsMicrovessel endothelial, pericyte, basement membrane and total mural area were greater in untreated diabetic animals than non-diabetic animals. Aldose reductase inhibitor treated diabetic animals had greater endothelial area and possibly pericyte area but not basement membrane or total mural area.ConclusionsThis study demonstrates that endoneurial microvessel abnormalities can be detected in experimental diabetic neuropathy. Microvessel basement membrane thickening will be prevented by an aldose reductase inhibitor. One mechanism by which abnormal polyol pathway activity may contribute to diabetic neuropathy could be through damage to microvessels.


Apmis ◽  
1996 ◽  
Vol 104 (1-6) ◽  
pp. 259-264 ◽  
Author(s):  
PETER S. OTURAI ◽  
RUTH RASCH ◽  
ERIK HASSELAGER ◽  
PETER B. JOHANSEN ◽  
HIROKI YOKOYAMA ◽  
...  

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