Skip Navigation
Skip to contents

Diabetes Metab J : Diabetes & Metabolism Journal

Search
OPEN ACCESS

Author index

Page Path
HOME > Browse > Author index
Search
Eun Young Lee  (Lee EY) 3 Articles
The Role of Glomerular Podocytes in Diabetic Nephropathy.
Eun Young Lee, Choon Hee Chung
Korean Diabetes J. 2007;31(6):451-454.   Published online November 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.6.451
  • 2,129 View
  • 19 Download
  • 3 Crossref
AbstractAbstract PDF
Diabetic nephropathy is the most common cause of end-stage renal disease and accounts for significant morbidity and mortality among individuals with diabetes mellitus. Therefore, the clarification of the pathogenesis of diabetic nephropathy is an urgent issue. Podocytes cover the outer layer of the glomerulus and maintain its integrity so that fluid and toxins exit in urine, but cells and important proteins are kept in the blood stream. Diabetes mellitus alters this structure, it becomes scarred and then the ability of the kidney to clear toxins is lost. Recent evidence shows that early in diabetes the podocyte number is reduced, areas of the glomerular basement membrane are denuded, and podocyte number predicts long-term urinary albumin excretion in the patients with diabetes and microalbuminuria. These results suggest that podocytes play a critical role in the early stage of diabetic nephropathy. It is the purpose of this article to review the pathogenetic role of podocytes in diabetic nephropathy.

Citations

Citations to this article as recorded by  
  • Inhibition of dipeptidyl peptidase-4 (DPP4), antioxidant, antiglycation and anti-inflammatory effect of Ferulic acid against streptozotocin toxicity mediate nephropathy in diabetic rats
    Maryam A. AL-Ghamdi, Said S. Moselhy
    Environmental Science and Pollution Research.2022; 30(12): 33942.     CrossRef
  • Study of Antiglycation, Hypoglycemic, and Nephroprotective Activities of the Green Dwarf Variety Coconut Water (Cocos nucifera L.) in Alloxan-Induced Diabetic Rats
    Isabella F.D. Pinto, Railmara P. Silva, Adriano de B. Chaves Filho, Lucas S. Dantas, Vanderson S. Bispo, Isaac A. Matos, Felipe A.M. Otsuka, Aline C. Santos, Humberto Reis Matos
    Journal of Medicinal Food.2015; 18(7): 802.     CrossRef
  • Effects of ferulic acid on diabetic nephropathy in a rat model of type 2 diabetes
    Ran Choi, Bo Hwan Kim, Jarinyaporn Naowaboot, Mi Young Lee, Mi Ri Hyun, Eun Ju Cho, Eun Soo Lee, Eun Young Lee, Young Chul Yang, Choon Hee Chung
    Experimental and Molecular Medicine.2011; 43(12): 676.     CrossRef
Effect of Peroxisome Proliferator Activated Receptor-gamma Agonist, Angiotensin II Receptor Blocker and alpha-lipoic Acid on Renal VEGF Expression in Diabetic Nephropathy.
Jang Hyun Koh, Yeon Lee, Mi Jin Kim, Young Goo Shin, Eun Young Lee, Choon Hee Chung
Korean Diabetes J. 2004;28(5):367-376.   Published online October 1, 2004
  • 1,072 View
  • 20 Download
AbstractAbstract PDF
BACKGROUND
Diabetic nephropathy is one of the most serious complications in diabetes mellitus, and it is the leading cause of end stage renal disease. It has been reported that angiotensin converting enzyme inhibitor (ACEi) reduces the vascular endothelial growth factor (VEGF) expression, and so it plays an important role in reducing the renal damage. Peroxisome proliferator activated receptor-gamma (PPAR-gamma) agonist is known to reduce insulin resistance in type 2 diabetic patients. In the previous study, PPAR-gamma agonist was shown to lower VEGF expression in the retina, but it increased the plasma VEGF level. Alpha-lipoic acid (alpha-LA), which is an antioxidant, lowers the increased level of VEGF in retina as well. The precise role of PPAR-gamma agonist and alpha-LA on renal VEGF expression in diabetic nephropathy is still uncertain. We studied the effect of PPAR-gamma agonist, angiotensin II receptor blocker (ATIIRB) and alpha-LA on the renal VEGF expression in diabetic rats. METHODS: We used 60 Sprague-Dawley male rats, those were 8 weeks old and weighted about 300 g each as the study subjects. Among them, 48 rats were chosen and injected with streptozotocin (70 mg/kg) into peritoneal cavity to induce diabetes mellitus. The rast were than divided into 5 groups. Group I was a normal control group (n=12), group II was diabetic control group (n=12), group III was diabetic group that was given with PPAR-gamma agonist (n=12), group IV was the diabetic group that was given ATIIRB (n=12), and group V was the diabetic rats that were given alpha-LA (n=12). We measured their body weight, blood glucose levels, 24 hour urine protein and albumin levels at the baseline, the 8th and the 16th weeks of the experiment. On the 16th weeks of our experiment we extracted the kidneys to measure the glomerular volume, the optical density of the VEGF staining and VEGF mRNA expression. RESULTS: At the beginning of the study, the 5 groups all showed similar 24 hour urine albumin levels. At the 8th week, group II showed an increased urine albumin level of 143.4 +/- 117.2 mg/day; this was greater than that of group IV (60.7+/-30.6 mg/day) (p<0.05). The glomerular volume and optical densities of VEGF expression were significantly reduced in group III, IV and V compared to group II. For group IV and V, the renal VEGF mRNA expression was significantly lower than that of group II, but group III showed no significant difference. from group II. CONCLUSION: Angiotensin II receptor blocker delayed the progression of diabetic nephropathy. PPAR-gamma agonist and alpha-lipoic acid did not have any protective effect against the progression of diabetic nephropathy in spite of the decreased VEGF expression noted in this study.
Mechanism of Podocyte Injury in Diabetic Nephropathy.
Eun Young Lee, Jae sook Song, Choon Hee Chung, Sae Yong Hong
Korean Diabetes J. 2003;27(4):343-351.   Published online August 1, 2003
  • 983 View
  • 26 Download
AbstractAbstract PDF
BACKGROUND
Since podocytes are involved in the maintenance of filtration barrier and normal structure in the kidney, podocyte injury can cause the disturbance of glomerular permselectivity and resultant proteinuria, and recent evidence shows that podocyte injury is associated with oxidative stress. However, the pathogenetic mechanism of podocyte injury in the development of diabetic nephropathy is not known. Thus, the present study examined the effect of high glucose level on cytoskeleton, slit diaphragm, podocyte-glomerular basement membrane interaction, and oxidative stress in cultured podocytes. METHODS: Differentiated cultured podocytes were used in this study. Quiescent cells were incubated with culture media containing 30 mM glucose for 48 hours. The amounts of integrin alpha3, vinculin, zona occludens (ZO)-1 and fibronectin protein expressed by podocytes were measured by Western blot analysis. Dichlorofluorescein diacetate-sensitive intracellular reactive oxygen species (ROS) were observed by confocal microscope and quantified by quantification software. Thiobarbituric acid reactive substances were also measured. Podocytes incubated with culture media containing 5.6 mM glucose were used as control. RESULTS: Integrin alpha3 expression was significantly decreased in podocytes cultured under high glucose level compared to control. However, vinculin and ZO-1 expressions were significantly increased in podocytes cultured under high glucose level compared to control. Fibronectin protein secreted by podocytes was also increased in podocytes cultured under high glucose level compared to control. ROS and thiobarbituric acid reactive substances in podocytes were also increased in high glucose medium compared to control. CONCLUSION: High glucose-induced oxidative stress and the changes of integrin a3, ZO-1 and vinculin lead to the alterations of cytoskeleton, intercellular or cell-matrix interactions. This podocyte injury may play a major role in the disturbance of the urinary filtration barrier and the development of proteinuria. These results confirmed the important role of podocyte injury in the development of diabetic nephropathy.

Diabetes Metab J : Diabetes & Metabolism Journal