Publication: Ultrastructural changes of pancreatic islets microcirculation in nonobese diabetic (NOD) mice.
Issued Date
2005-12-01
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ISSN
01251562
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2-s2.0-33646189715
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Mahidol University
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SCOPUS
Bibliographic Citation
The Southeast Asian journal of tropical medicine and public health.. Vol.36 Suppl 4, (2005), 274-278
Suggested Citation
Navakanit Sachanonta, Emsri Pongponratn, Raywadee Butraporn, Urai Chaisri, Benjama Saelim, Virat Sumeteewatanakul, Ticomporn Yamsaad, Nut Sawadrat Ultrastructural changes of pancreatic islets microcirculation in nonobese diabetic (NOD) mice.. The Southeast Asian journal of tropical medicine and public health.. Vol.36 Suppl 4, (2005), 274-278. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/16656
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Title
Ultrastructural changes of pancreatic islets microcirculation in nonobese diabetic (NOD) mice.
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Abstract
The objective of this study was to investigate the ultrastructural changes of vascular pancreatic islets using a transmission electron microscopic technique. The major ultrastructural changes of microvessel in NOD mice are indicated by the swelling and vacuolization of the endothelial cell. Swollen cells are the first noticeable lesion of the cell response in reversible degeneration that is caused by the failure of homeostatic control. Loss in endothelial cell homeostasis is primarily a marker of endothelial dysfunction that plays a key role in the pathogenesis of diabetic vascular disease by losing the control of vascular tone. Diabetes also associates with an increased generation of oxygen-derived free radicals that may impair vasodilatation through the inactivation of vasodilators. In conclusion, consistent with a hypothesis that loss of the modulatory role of the endothelium may be a critical and initiating factor in the development of diabetic vascular disease, the ultrastructural changes in this study may indicate the first sign of endothelial dysfunction. This dysfunction correlates to the relationship between diabetes and reversible lesions of vessels in NOD mice, making for a better understanding of the pathophysiology of diabetic vascular disease to set the stage for further investigation to restore endothelial dysfunction in diabetes.