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Original Article
Complications
Lipid Abnormalities in Type 2 Diabetes Mellitus Patients with Overt Nephropathy
Sabitha Palazhy, Vijay Viswanathan
Diabetes Metab J. 2017;41(2):128-134.   Published online January 11, 2017
DOI: https://doi.org/10.4093/dmj.2017.41.2.128
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  • 32 Web of Science
  • 36 Crossref
AbstractAbstract PDFPubReader   
Background

Diabetic nephropathy is a major complication of diabetes and an established risk factor for cardiovascular events. Lipid abnormalities occur in patients with diabetic nephropathy, which further increase their risk for cardiovascular events. We compared the degree of dyslipidemia among type 2 diabetes mellitus (T2DM) subjects with and without nephropathy and analyzed the factors associated with nephropathy among them.

Methods

In this retrospective study, T2DM patients with overt nephropathy were enrolled in the study group (n=89) and without nephropathy were enrolled in the control group (n=92). Both groups were matched for age and duration of diabetes. Data on total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), urea and creatinine were collected from the case sheets. TG/HDL-C ratio, a surrogate marker for small, dense, LDL particles (sdLDL) and estimated glomerular filtration rate (eGFR) were calculated using equations. Multivariate analysis was done to determine the factors associated with eGFR.

Results

Dyslipidemia was present among 56.52% of control subjects and 75.28% of nephropathy subjects (P=0.012). The percentage of subjects with atherogenic dyslipidemia (high TG+low HDL-C+sdLDL) was 14.13 among controls and 14.61 among nephropathy subjects. Though serum creatinine was not significantly different, mean eGFR value was significantly lower among nephropathy patients (P=0.002). Upon multivariate analysis, it was found that TC (P=0.007) and HDL-C (P=0.06) were associated with eGFR among our study subjects.

Conclusion

Our results show that dyslipidemia was highly prevalent among subjects with nephropathy. Regular screening for dyslipidemia may be beneficial in controlling the risk for adverse events among diabetic nephropathy patients.

Citations

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Review
Complications
Autophagy: A Novel Therapeutic Target for Diabetic Nephropathy
Shinji Kume, Daisuke Koya
Diabetes Metab J. 2015;39(6):451-460.   Published online December 11, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.6.451
  • 5,159 View
  • 57 Download
  • 80 Web of Science
  • 77 Crossref
AbstractAbstract PDFPubReader   

Diabetic nephropathy is a leading cause of end stage renal disease and its occurance is increasing worldwide. The most effective treatment strategy for the condition is intensive treatment to strictly control glycemia and blood pressure using renin-angiotensin system inhibitors. However, a fraction of patients still go on to reach end stage renal disease even under such intensive care. New therapeutic targets for diabetic nephropathy are, therefore, urgently needed. Autophagy is a major catabolic pathway by which mammalian cells degrade macromolecules and organelles to maintain intracellular homeostasis. The accumulation of damaged proteins and organelles is associated with the pathogenesis of diabetic nephropathy. Autophagy in the kidney is activated under some stress conditions, such as oxidative stress and hypoxia in proximal tubular cells, and occurs even under normal conditions in podocytes. These and other accumulating findings have led to a hypothesis that autophagy is involved in the pathogenesis of diabetic nephropathy. Here, we review recent findings underpinning this hypothesis and discuss the advantages of targeting autophagy for the treatment of diabetic nephropathy.

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Original Articles
Prevalence and Determinants of Diabetic Nephropathy in Korea: Korea National Health and Nutrition Examination Survey
Jae Hee Ahn, Ji Hee Yu, Seung-Hyun Ko, Hyuk-Sang Kwon, Dae Jung Kim, Jae Hyeon Kim, Chul Sik Kim, Kee-Ho Song, Jong Chul Won, Soo Lim, Sung Hee Choi, Kyungdo Han, Bong-Yun Cha, Nan Hee Kim
Diabetes Metab J. 2014;38(2):109-119.   Published online April 18, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.2.109
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AbstractAbstract PDFPubReader   
Background

Diabetic nephropathy is a leading cause of end stage renal disease and is associated with an increased risk of cardiovascular mortality. It manifests as albuminuria or impaired glomerular filtration rate (GFR), and the prevalence of diabetic nephropathy varies with ethnicity. The prevalence of diabetic nephropathy and its determinants in Korean adults have not previously been studied at the national level. This cross-sectional study was undertaken to ascertain the prevalence and determinants of albuminuria and chronic kidney disease (CKD) in Korean patients with diabetes.

Methods

The Korea National Health and Nutrition Examination Survey (KNHANES) V, conducted in 2011, was used to define albuminuria (n=4,652), and the dataset of KNHANES IV-V (2008-2011) was used to define CKD (n=21,521). Selected samples were weighted to represent the entire civilian population in Korea. Albuminuria was defined as a spot urine albumin/creatinine ratio >30 mg/g. CKD was defined as a GFR <60 mL/min/1.73 m2.

Results

Among subjects with diabetes, 26.7% had albuminuria, and 8.6% had CKD. Diabetes was associated with an approximate 2.5-fold increased risk of albuminuria, with virtually no difference between new-onset and previously diagnosed diabetes. Only systolic blood pressure was significantly associated with albuminuria, and old age, high serum triglyceride levels, and previous cardiovascular disease (CVD) were related with CKD in subjects with diabetes.

Conclusion

Korean subjects with diabetes had a higher prevalence of albuminuria and CKD than those without diabetes. Blood pressure was associated with albuminuria, and age, triglyceride level, and previous CVD were independent determinants of CKD in subjects with diabetes.

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    Genes & Genomics.2016; 38(7): 573.     CrossRef
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    J.‐S. Yun, Y.‐B. Ahn, K.‐H. Song, K.‐D. Yoo, Y.‐M. Park, H.‐W. Kim, S.‐H. Ko
    Diabetic Medicine.2016; 33(5): 639.     CrossRef
  • The association between abnormal heart rate variability and new onset of chronic kidney disease in patients with type 2 diabetes: A ten-year follow-up study
    Jae-Seung Yun, Yu-Bae Ahn, Ki-Ho Song, Ki-Dong Yoo, Hyung-Wook Kim, Yong-Moon Park, Seung-Hyun Ko
    Diabetes Research and Clinical Practice.2015; 108(1): 31.     CrossRef
  • Central obesity is an independent risk factor for microalbuminuria in both the general Korean women and nondiabetic nonhypertensive subpopulation: Association of microalbuminuria and metabolic syndrome from the Korea National Health and Nutrition Examinat
    John Hoon Rim, Yong-ho Lee, Bong-Soo Cha, Sang-Guk Lee, Jeong-Ho Kim
    Clinica Chimica Acta.2015; 448: 74.     CrossRef
  • Diabetic Kidney Disease: From Epidemiology to Clinical Perspectives
    Cheol Whee Park
    Diabetes & Metabolism Journal.2014; 38(4): 252.     CrossRef
Effect of Eplerenone, a Selective Aldosterone Blocker, on the Development of Diabetic Nephropathy in Type 2 Diabetic Rats
Jae Hee Ahn, Ho Cheol Hong, Myong Jin Cho, Yoon Jung Kim, Hae Yoon Choi, Chai Ryoung Eun, Sae Jeong Yang, Hye Jin Yoo, Hee Young Kim, Ji A Seo, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Dong Seop Choi, Nan Hee Kim
Diabetes Metab J. 2012;36(2):128-135.   Published online April 17, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.2.128
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AbstractAbstract PDFPubReader   
Background

Aldosterone antagonists are reported to have beneficial effects on diabetic nephropathy by effective blocking of the renin-angiotensin-aldosterone system. We investigated the renoprotective effect of the selective aldosterone receptor blocker eplerenone, the angiotensin converting enzyme inhibitor lisinopril, and combined eplerenone and lisinopril treatment in type 2 diabetic rats.

Methods

Animals were divided into six groups as follows: Otsuka Long-Evans Tokushima Fatty (OLETF) rat control, OLETF rats treated with a low dose of eplerenone (50 mg/kg/day), OLETF rats treated with a high dose of eplerenone (200 mg/kg/day), OLETF rats treated with lisinopril (10 mg/kg/day), OLETF rats treated with a combination of both drugs (eplerenone 200 mg/kg/day and lisinopril 10 mg/kg/day), and obese non-diabetic Long-Evans Tokushima Otsuka rats for 26 weeks.

Results

Urinary albumin excretion was significantly lower in the lisinopril group, but not in the eplerenone group. Urinary albumin excretion was decreased in the combination group than in the lisinopril group. Glomerulosclerosis and renal expression of type I and type IV collagen, plasminogen activator inhibitor-1, transforming growth factor-β1, connective tissue growth factor, and fibronectin mRNA were markedly decreased in the lisinopril, eplerenone, and combination groups.

Conclusion

Eplerenone and lisinopril combination showed additional benefits on type 2 diabetic nephropathy compared to monotherapy of each drug.

Citations

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  • Up-Date on Diabetic Nephropathy
    Maria Chiara Pelle, Michele Provenzano, Marco Busutti, Clara Valentina Porcu, Isabella Zaffina, Lucia Stanga, Franco Arturi
    Life.2022; 12(8): 1202.     CrossRef
  • The role of free radical oxidation in the kidneys in the nephroprotective action of eplerenone, a mineralocorticoid receptor antagonist, in experimental diabetes mellitus
    A. Yu. Zharikov, S. O. Filinova, O. N. Mazko, O. G. Makarova, I. P. Bobrov, V. M. Bryukhanov
    Bulletin of Siberian Medicine.2021; 20(2): 29.     CrossRef
  • Effect of Mineralocorticoid Receptor Antagonism and ACE Inhibition on Angiotensin Profiles in Diabetic Kidney Disease: An Exploratory Study
    Johannes J. Kovarik, Christopher C. Kaltenecker, Oliver Domenig, Marlies Antlanger, Marko Poglitsch, Chantal Kopecky, Marcus D. Säemann
    Diabetes Therapy.2021; 12(9): 2485.     CrossRef
  • Diabetic nephropathy: An update on pathogenesis and drug development
    Vikram Rao A/L B Vasanth Rao, Sean Hong Tan, Mayuren Candasamy, Subrat Kumar Bhattamisra
    Diabetes & Metabolic Syndrome: Clinical Research & Reviews.2019; 13(1): 754.     CrossRef
  • Effects of mineralocorticoid receptor antagonists on the progression of diabetic nephropathy
    Li‐Jing Sun, Yan‐Ni Sun, Jian‐Ping Shan, Geng‐Ru Jiang
    Journal of Diabetes Investigation.2017; 8(4): 609.     CrossRef
  • New agents modulating the renin-angiotensin-aldosterone system—Will there be a new therapeutic option?
    Anna Gromotowicz-Poplawska, Piotr Szoka, Patrycjusz Kolodziejczyk, Karol Kramkowski, Marzena Wojewodzka-Zelezniakowicz, Ewa Chabielska
    Experimental Biology and Medicine.2016; 241(17): 1888.     CrossRef
  • Crosstalk between peroxisome proliferator-activated receptor-γ and mineralcorticoid receptor in TNF-α activated renal tubular cell
    Jing Xiao, Weijun Chen, Yijun Lu, Xiaoli Zhang, Chensheng Fu, Zhenwen Yan, Zhenxing Zhang, Zhibin Ye
    Inflammation Research.2015; 64(8): 603.     CrossRef
  • Eplerenone reduces arterial thrombosis in diabetic rats
    Agnieszka Zakrzeska, Anna Gromotowicz-Popławska, Janusz Szemraj, Piotr Szoka, Wioleta Kisiel, Tomasz Purta, Irena Kasacka, Ewa Chabielska
    Journal of the Renin-Angiotensin-Aldosterone System.2015; 16(4): 1085.     CrossRef
  • Pharmacological modulation of fibrinolytic response – In vivo and in vitro studies
    Karol Kramkowski, Agnieszka Leszczynska, Wlodzimierz Buczko
    Pharmacological Reports.2015; 67(4): 695.     CrossRef
Effects of Spironolactone and Losartan on Diabetic Nephropathy in a Type 2 Diabetic Rat Model
Mi Young Lee, Myoung Sook Shim, Bo Hwan Kim, Soon Won Hong, Ran Choi, Eun Young Lee, Soo Min Nam, Gun Woo Kim, Jang Yel Shin, Young Goo Shin, Choon Hee Chung
Diabetes Metab J. 2011;35(2):130-137.   Published online April 30, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.2.130
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AbstractAbstract PDFPubReader   
Background

While there is an evidence that the anti-inflammatory properties of spironolactone can attenuate proteinuria in type 2 diabetes, its effects on vascular endothelial growth factor (VEGF) expression in diabetic nephropathy have not been clearly defined. In this study, we examined the effects of spironolactone, losartan, and a combination of these two drugs on albuminuria, renal VEGF expression, and inflammatory and oxidative stress markers in a type 2 diabetic rat model.

Methods

Thirty-three Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats were divided into four groups and treated with different medication regimens from weeks 25 to 50; OLETF diabetic controls (n=5), spironolactone-treated (n=10), losartan-treated (n=9), and combination of spironolactone- and losartan-treated (n=9).

Results

At week 50, the albumin-to-creatinine ratio was significantly decreased in the losartan and combination groups compared to the control OLETF group. No decrease was detected in the spironolactone group. There was a significant reduction in renal VEGF, transforming growth factor (TGF)-β, and type IV collagen mRNA levels in the spironolactone- and combination regimen-treated groups. Twenty-four hour urine monocyte chemotactic protein-1 levels were comparable in all four groups but did show a decreasing trend in the losartan and combination regimen groups. Twenty-four hour urine malondialdehyde levels were significantly decreased in the spironolactone- and combination regimen-treated groups.

Conclusion

These results suggest that losartan alone and a combined regimen of spironolactone and losartan could ameliorate albuninuria by reducing renal VEGF expression. Also, simultaneous treatment with spironolactone and losartan may have protective effects against diabetic nephropathy by decreasing TGF-β and type IV collagen expression and by reducing oxidative stress in a type 2 diabetic rat model.

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  • Tetrahydrocurcumin Add‐On therapy to losartan in a rat model of diabetic nephropathy decreases blood pressure and markers of kidney injury
    Mahyar Khazaeli, Ane C. F. Nunes, Yitong Zhao, Mahziar Khazaali, John Prudente, Nosratola D. Vaziri, Bhupinder Singh, Wei Ling Lau
    Pharmacology Research & Perspectives.2023;[Epub]     CrossRef
  • Type 2 Diabetes Mellitus: Pathogenic Features and Experimental Models in Rodents
    Inessa G. Gvazava, M. V. Karimova, A. V. Vasiliev, E. A. Vorotelyak
    Acta Naturae.2022; 14(3): 57.     CrossRef
  • Role of mineralocorticoid receptor antagonists in kidney diseases
    Vishal Patel, Amit Joharapurkar, Mukul Jain
    Drug Development Research.2021; 82(3): 341.     CrossRef
  • Multi-strain probiotic supplement attenuates streptozotocin-induced type-2 diabetes by reducing inflammation and β-cell death in rats
    Pei-Shan Hsieh, Hsieh-Hsun Ho, Shu Ping Tsao, Shih-Hung Hsieh, Wen-Yang Lin, Jui-Fen Chen, Yi-Wei Kuo, Shin-Yu Tsai, Hui-Yu Huang, Michael W. Greene
    PLOS ONE.2021; 16(6): e0251646.     CrossRef
  • Ocular surface complications in diabetes: The interrelationship between insulin and enkephalin
    Indira Purushothaman, Ian S. Zagon, Joseph W. Sassani, Patricia J. McLaughlin
    Biochemical Pharmacology.2021; 192: 114712.     CrossRef
  • Mineralocorticoid Receptor Antagonists in Diabetic Kidney Disease
    Daiji Kawanami, Yuichi Takashi, Yoshimi Muta, Naoki Oda, Dai Nagata, Hiroyuki Takahashi, Makito Tanabe
    Frontiers in Pharmacology.2021;[Epub]     CrossRef
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    Devesh Aggarwal, Gaaminepreet Singh
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  • Bioactive Agent Discovery from the Natural Compounds for the Treatment of Type 2 Diabetes Rat Model
    Shih-Chun Yang, Ching-Yun Hsu, Wei-Ling Chou, Jia-You Fang, Shih-Yi Chuang
    Molecules.2020; 25(23): 5713.     CrossRef
  • Losartan improves renal function and pathology in obese ZSF-1 rats
    Zhi Su, Deborah Widomski, Arthur Nikkel, Laura Leys, Marian Namovic, Diana Donnelly-Roberts, Murali Gopalakrishnan, Steve McGaraughty
    Journal of Basic and Clinical Physiology and Pharmacology.2018; 29(3): 281.     CrossRef
  • Analyzing polymeric nanofibrous scaffold performances in diabetic animal models for translational chronic wound healing research
    Nowsheen Goonoo, Archana Bhaw-Luximon
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  • Stimulatory effect of insulin on renal proximal tubule sodium transport is preserved in type 2 diabetes with nephropathy
    Motonobu Nakamura, Nobuhiko Satoh, Masashi Suzuki, Haruki Kume, Yukio Homma, George Seki, Shoko Horita
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  • Combination therapy with spironolactone and candesartan protects against streptozotocin-induced diabetic nephropathy in rats
    Amal Hofni, Mohamed A. El-Moselhy, Ashraf Taye, Mohamed M. Khalifa
    European Journal of Pharmacology.2014; 744: 173.     CrossRef
  • Renal Protective Role of Xiexin Decoction with Multiple Active Ingredients Involves Inhibition of Inflammation through Downregulation of the Nuclear Factor-κB Pathway in Diabetic Rats
    Jia-sheng Wu, Rong Shi, Jie Zhong, Xiong Lu, Bing-liang Ma, Tian-ming Wang, Bin Zan, Yue-ming Ma, Neng-neng Cheng, Fu-rong Qiu
    Evidence-Based Complementary and Alternative Medicine.2013; 2013: 1.     CrossRef
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    Aileen JF King
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  • Effect of Eplerenone, a Selective Aldosterone Blocker, on the Development of Diabetic Nephropathy in Type 2 Diabetic Rats
    Jae Hee Ahn, Ho Cheol Hong, Myong Jin Cho, Yoon Jung Kim, Hae Yoon Choi, Chai Ryoung Eun, Sae Jeong Yang, Hye Jin Yoo, Hee Young Kim, Ji A Seo, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Dong Seop Choi, Nan Hee Kim
    Diabetes & Metabolism Journal.2012; 36(2): 128.     CrossRef
Association Study of the Peroxisome Proliferators-Activated Receptor gamma2 Pro12Ala Polymorphism with Diabetic Nephropathy.
Kyu Ho Lee, Hee Seog Jeong, Khan Young Choi, Hyun Kim, Dal Sic Lee, Ji Young Kang, Hyun Jeong Jeon, Tae Keun Oh
Korean Diabetes J. 2008;32(5):402-408.   Published online October 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.5.402
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AbstractAbstract PDF
BACKGROUND
Peroxisome proliferators-activated receptor gamma (PPARgamma) is a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors and known to play a role in regulating the expression of numerous genes involved in lipid metabolism, metabolic syndrome, inflammation, and atherosclerosis. The PPARgamma2 Pro12Ala polymorphism has recently been shown to be associated with diabetic nephropathy. In this study, we evaluated the relationship between PPARgamma2 Pro12Ala polymorphism and type 2 diabetic nephropathy whose duration of diabetes was over 10 years. METHODS: We conducted a case-control study, which enrolled 367 patients with type 2 diabetes. Genotyping of PPARgamma2 Pro12Ala polymorphism was performed using polymerase chain reaction followed by digestion with Hae III restriction enzyme. RESULTS: The genotype or allele frequencies of PPARgamma2 Pro12Ala polymorphism were not significantly different in diabetic patients with or without diabetic nephropathy. The genotype frequencies in terms of diabetic retinopathy and macrovascular complications such as coronary artery disease or stroke were not different either. Interestingly, nephropathy patients with Ala/Pro genotype showed lower C-peptide levels than those of Pro/Pro genotype. CONCLUSION: Our results suggest that PPARgamma2 Pro12Ala polymorphism is not associated with diabetic nephropathy in type 2 diabetic patients.
Clinical Significance of Decreased Glomerular Filtration Rate (GFR) without Albuminuria among Type 2 Diabetics.
Ji Eun Lee, Kyu Chang Won, Hyoung Woo Lee, Ji Sung Yoon
Korean Diabetes J. 2008;32(3):252-258.   Published online June 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.3.252
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AbstractAbstract PDF
BACKGROUND
Microalbuminuria in type 2 diabetes is a predictor of development of clinical nephropathy and cardiovascular disease. But, it has been reported that reduced glomerular filtration rate (GFR) may occur in some normoalbuminuric diabetic patients. The aim of this study was to identify whether decreased GFR without microalbuminuria is to predict diabetic vascular complications. METHODS: Between January 1998 and February 2001, 73 patients with type 2 diabetes who visited Yeungnam university medical center were divided into 5 groups according to initial GFR ranges: group 1 (GFR < 30 mL/min), group 2 (30 < or = GFR < 60 mL/min), group 3 (60 < or = GFR < 90 mL/min), group 4 (90 < or = GFR < 125 mL/min), group 5 (125 mL/min < or = GFR). They were examined for microvascular and macrovascular complications initially and after 4 years. RESULTS: Decreased GFR had a negative correlation with age (r = -0.472, P = 0.001). Decreased GFR without microalbuminuria had a significant correlation with development of diabetic nephropathy (P = 0.016) after 4 years. There were no significant correlation with the prevalence of diabetic retinopathy, peripheral neuropathy, and macrovacular disease. But, our study showed that coronary artery disease had an increasing tendency with decreased GFR without statistical significance (P = 0.085). CONCLUSIONS: Our data suggest that reduced GFR, independent of albuminuria, may be an important predictor of diabetic nephropathy and coronary artery disease to some extent. So we recommend that not only the microalbuminuria, but also the decrease in GFR should be evaluated at the follow-up of patients with type 2 diabetes.

Citations

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  • Screening and Management of Diabetic Nephropathy
    Ji Sung Yoon
    The Journal of Korean Diabetes.2013; 14(1): 19.     CrossRef
Protective Effects of Lithospermic Acid B on Diabetic Nephropathy in OLETF Rats Comparing with Amlodipine and Losartan.
Eun Seok Kang, Beom Seok Kim, Chul Hoon Kim, Gi Ho Seo, Seung Jin Han, Sung Wan Chun, Kyu Yeon Hur, Chul Woo Ahn, Hunjoo Ha, Mankil Jung, Bong Soo Cha, Hyun Chul Lee
Korean Diabetes J. 2008;32(1):10-20.   Published online February 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.1.10
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Lithospermic acid B (LAB), an active component isolated from Salvia miltiorrhizae, has been reported to have renoprotective effects in type 1 and type 2 diabetic animal models. We examined the effects of LAB on the prevention of diabetic nephropathy compared with amlodipine, a calcium channel blocker, and losartan, an angiotensin receptor blocker, in Otsuka Long-Evans-Tokushima Fatty (OLETF) rats, an animal model of type 2 diabetes. METHODS: LAB (20 mg/kg), amlodipine (10 mg/kg), or losartan (10 mg/kg) was given orally once daily to 10-week-old male OLETF rats for 28 weeks. RESULTS: None of LAB, losartan, and amlodipine exhibited effects on blood glucose levels. Treatment with amlodipine or losartan resulted in similar reductions in blood pressure; however, LAB was less effective in lowering blood pressure. Albuminuria was markedly suppressed by losartan and LAB, but not by amlodipine. LAB treatment decreased levels of renal lipid peroxidation, monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor-beta1 (TGF-beta1). CONCLUSION: These results suggest that LAB has beneficial effects on the diabetic nephropathy in OLETF rats by decreasing oxidative stress and inflammation as potent as losartan.

Citations

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  • An Overview on Naturally Occurring Phytoconstituent: Lithospermic Acid
    Bhupesh Chander Semwal, Amjad Hussain, Sonia Singh
    The Natural Products Journal.2024;[Epub]     CrossRef
Review
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
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  • 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.

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  • 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
Original Articles
Activation of NF-kappaB and AP-1 in Peripheral Blood Mononuclear Cells Isolated from Patients with Diabetic Nephropathy.
Jisun Nam, Min Ho Cho, Jong Suk Park, Geun Taek Lee, Hai Jin Kim, Eun Seok Kang, Yu Mie Lee, Chul Woo Ahn, Bong Soo Cha, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hun Joo Ha, Hyun Chul Lee
Korean Diabetes J. 2007;31(3):261-273.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.261
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AbstractAbstract PDF
BACKGROUND
We evaluated the role of oxidative stress in diabetic nephropathy by measuring intracellular reactive oxygen species (ROS) and redox-sensitive transcription factors in isolated peripheral mononuclear cells (PBMC). METHODS: From 66 diabetic patients with or without diabetic nephropathy (Group III and II, respectively) and 49 normal control subjects (Group I), spontaneous and stimulated ROS levels, activities of nuclear factor-kappa B (NF-kappaB), activator protein-1 (AP-1), and specificity protein1 (Sp1) in PBMC, urinary and PBMC TGF-beta1 (transforming growth factor-beta1), and 24-hour urinary albumin excretion (UAE) were measured. RESULTS: Spontaneous ROS was significantly higher in group III and II than group I (60.7 +/- 3.3 vs. 60.0 +/- 3.0 vs. 41.1 +/- 2.4%, respectively), and stimulated ROS were significantly higher in Group III compared to Group II (Increment of H2O2-induced ROS production: 21.8 +/- 2.2 vs. 11.1 +/- 2.0%, respectively; increment of PMA-induced ROS production 23.5 +/- 4.5 vs. 21.6 +/- 2.2%, respectively). The activities of NF-kappaB and AP-1, but not of Sp1, were significantly higher in Group III than in Group II (2.53 vs. 2.0 vs. 1.43-fold, respectively). Both PBMC- and urinary TGF-beta1 levels were higher in Group III than Group II (3.23 +/- 0.39 vs. 1.99 +/- 0.68 ng/mg in PBMCs, 16.88 +/- 6.84 vs. 5.61 +/- 1.57 ng/mL in urine, both respectively), and they were significantly correlated with activities of NF-kappaB and AP-1 and 24-hour UAE. CONCLUSIONS: Increased intracellular ROS generation in PBMCs of diabetic patients is involved in the pathogenesis of diabetic nephropathy through activation of NF-kappaB and AP-1, but not Sp1, and increased expression of TGF-beta1.
Effects of Troglitazone on the Expression of VEGF and TGF-beta in Cultured Rat Mesangial Cells.
Dong Lim Kim, Nan Hee Kim, Dong Seop Choi
Korean Diabetes J. 2007;31(3):220-229.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.220
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AbstractAbstract PDF
BACKGROUND
Clinical study reported that troglitazone ameliorated microalbuminuria in diabetic nephropathy. However, the mechanism of action is not fully understood. Vascular endothelial growth factor (VEGF) is known as vascular permeability factor and it is considered the most likely cause of glomerular hyperfiltration and proteinuria in diabetic nephropathy. Transforming growth factor-beta (TGF-beta) is a potent inducer of extracellular matrix production and fibrosis in renal cells and one of the important cytokine in the pathogenesis of diabetic nephropathy. To determine whether troglitazone affects VEGF and TGF-beta production in diabetic nephropathy, we examined the effects of troglitazone on the VEGF and TGF-beta expression in cultured rat mesangial cells exposed to high glucose concentration. METHODS: Rat mesangial cells were cultured in media with D-glucose 5.5 mM (NG) or D-glucose 30 mM (HG), or D-glucose 30 mM/troglitazone 20 micrometer(HTz) and for 6, 24, or 72 hours, respectively. VEGF and TGF-beta expression were assessed by semiquantitative RT-PCR and western blot analysis. RESULTS: Troglitazone decreased the VEGF164 and VEGF120 mRNA expressions in cultured rat mesangial cells exposed to high glucose concentration with incubation for 24 and 72 hours, respectively. VEGF protein was also decreased in experimental group treated with troglitazone (HTz) than in those with HG for 24 and 72 hours. However troglitazone had no effect on the expression of TGF-beta mRNA in mesangial cells. CONCLUSION: This study suggested that troglitazone may modulate the development and progression of diabetic nephropathy by reducing the expression of VEGF in mesangial cells
Transforming Growth Factor-beta 1 Gene Polymorphisms According to Diabetic Nephropathy in Type 2 Diabetes.
Hyun Jeong Jeon, Ok Hee Kim, Kil Ho, Soon Kil Kwon, Tae Keun Oh
Korean Diabetes J. 2007;31(2):144-150.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.144
  • 1,457 View
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AbstractAbstract PDF
BACKGROUND
Transforming growth factor-beta is known to play a role in the interaction between metabolic and hemodynamic factors in mediating accumulation of extracellular matrix in the diabetic nephropathy. TGF-beta1 gene polymorphism was associated with circulating TGF-beta levels and influenced the pathogenesis of fibrotic diseases including diabetic nephropathy. In this study, we examined the relationship between TGF-beta1 gene codon 10 polymorphism and type 2 diabetic nephropathy with more than 10-year history of disease. METHODS: We conducted a case-control study, which enrolled 325 type 2 diabetes. A total of 176 patients with diabetic nephropathy were compared with 149 patients without diabetic nephropathy. TGF-beta1 codon 10 genotyping was determined using polymerase chain reaction with sequence specific primers method. RESULTS: Distribution of TGF-beta1 codon 10 genotype in the patients either with nephropathy or without nephropathy is confined to Hardy-Weinberg equilibrium. The patients with nephropathy have higher frequency of TGF-beta1 GA/GG genotypes than the patients without nephropathy [GA/GG:AA = 119 (67.6%) : 57 (32.4%) vs. 80 (53.7%) : 69 (46.3%), P < 0.05]. Among patients with diabetic nephropathy, those with TGF-beta1 GA/GG genotypes had higher serum levels of total cholesterol and LDL-cholesterol. CONCLUSION: Our results suggest that TGF-beta1 gene codon 10 polymorphism may contribute to the type 2 diabetic nephropathy.
The Effect of High Glucose and TGF-beta on the Cellular Injury in Cultured Glomerular Epithelial Cells.
Gui Hwa Jeong, Sung Chang Chung, Eui Dal Jung, Yun Jeong Doh, Hee Kyoung Kim, Soon Hong Park, In Hae Park, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim, In Kyu Lee, Cheol Woo Ko
Korean Diabetes J. 2006;30(4):254-263.   Published online July 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.4.254
  • 1,875 View
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AbstractAbstract PDF
BACKGROUND
The glomerulus is a complex physiological structure, as well as selective filtration barrier in the control of renal blood flow and blood pressure. Glomerular epithelial cells may play an important role in development of diabetic nephropathy. Apoptosis of the glomerular epithelial cells are characterized by disappearance of a selective filtration barrier. TGF-beta is a key factor in the development of diabetic nephropathy because of its effects on the accumulation of extracellular matrix and mesangial cell proliferation. We examined whether the high glucose and TGF-beta induce the apoptosis in cultured rat glomerular epithelial cells. METHODS: Glomerular epithelial cells were cultured from rat glomeruli and conditioned with different concentration of TGF-beta or high-glucose. We measured apoptosis of cultured rat glomerular epithelial cell conditioning with different concentration of TGF-beta or high-glucose by using DNA electrophoresis. RESULTS: High glucose (25 mM) induced apoptosis of cultured rat glomerular epithelial cells compared to controls. TGF-beta also induced cell death of cultured rat glomerular epithelial cells in dose dependent manner. CONCLUSION: These results suggest that high glucose and TGF-beta-induced cell death of glomerular epithelial cell may play an important role in diabetic nephropathy and proteinuria. Pathway of apoptosis or cell death by high glucose and TGF-beta must be investigated in the glomerular epithelial cells.
Protective Effects of Lithospermate B on Diabetic Nephropathy in OLETF Rat.
Hyun Joo Lee, Geun Taek Lee, Eun Seok Kang, Kyu Yeon Hur, Zheng Shan Zhao, Chul Woo Ahn, Hun Joo Ha, Man Kil Jung, Bong Soo Cha, Hyun Chul Lee
Korean Diabetes J. 2005;29(4):322-332.   Published online July 1, 2005
  • 1,053 View
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AbstractAbstract PDF
BACKGROUND
Magnesium lithospermate B(LAB), an active component isolated from Salvia milltiorrhizae, has been reported to have renoprotective effects in type 1 diabetic animal model. The purpose of this study was to examine the effects of LAB on the prevention of diabetic nephropathy in Otsuka Long-Evans Tokushima Fatty(OLETF) rat which is regarded as an animal model of type 2 diabetes. METHODS: Ten microgram of LAB/kg or Vehicle(PBS) was given orally once daily to 10-week-old male OLETF rats and LETO rats for 40 weeks. Intra-peritoneal glucose tolerance test was performed at 50 weeks. 24 hr urinary protein excretion amounts were measured. Lipid peroxidation, TGF-beta1 and ED-1 of renal cortex were measured. RESULTS: The mean body weight of LAB+OLETF was not significantly different from that of OLETF rats. LAB treatment decreased proteinuria, lipid peroxidation, and free fatty acid in OLETF rats without decrease in the plasma glucose concentration. Also, LAB inhibited the progression of glomerular hypertrophy and mesangial expansion. LAB effectively decreased ED-1 positive cells, ECM expansion, and TGF-beta1 level in the renal cortex of OLETF rats. CONCLUSIONS: These results suggest that the beneficial effects of LAB on the diabetic renal damage in the OLETF rats may depend on a mechanism of decreasing oxidative stress. LAB might be a new therapeutic agent for the prevention of nephropathy in type 2 diabetes as well as type 1 diabetes.
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
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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.

Diabetes Metab J : Diabetes & Metabolism Journal
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