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Renal Tubular Damage Marker, Urinary N-acetyl-β-D-Glucosaminidase, as a Predictive Marker of Hepatic Fibrosis in Type 2 Diabetes Mellitus
Hae Kyung Kim, Minyoung Lee, Yong-ho Lee, Eun Seok Kang, Bong-Soo Cha, Byung-Wan Lee
Diabetes Metab J. 2022;46(1):104-116.   Published online July 13, 2021
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  • 195 Download
  • 4 Web of Science
  • 5 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Non-alcoholic steatohepatitis is closely associated with the progression of diabetic kidney disease (DKD) in type 2 diabetes mellitus (T2DM). We investigated whether urinary N-acetyl-β-D-glucosaminidase (u-NAG), an early renal tubular damage biomarker in DKD, could be related to the degree of hepatic fibrosis in patients with T2DM.
A total of 300 patients with T2DM were enrolled in this study. Hepatic steatosis and fibrosis were determined using transient elastography. The levels of urinary biomarkers, including u-NAG, albumin, protein, and creatinine, and glucometabolic parameters were measured.
Based on the median value of the u-NAG to creatinine ratio (u-NCR), subjects were divided into low and high u-NCR groups. The high u-NCR group showed a significantly longer duration of diabetes, worsened hyperglycemia, and a more enhanced hepatic fibrosis index. A higher u-NCR was associated with a greater odds ratio for the risk of higher hepatic fibrosis stage (F2: odds ratio, 1.99; 95% confidence interval [CI], 1.04 to 3.82). Also, u-NCR was an independent predictive marker for more advanced hepatic fibrosis, even after adjusting for several confounding factors (β=1.58, P<0.01).
The elevation of u-NAG was independently associated with a higher degree of hepatic fibrosis in patients with T2DM. Considering the common metabolic milieu of renal and hepatic fibrosis in T2DM, the potential use of u-NAG as an effective urinary biomarker reflecting hepatic fibrosis in T2DM needs to be validated in the future.


Citations to this article as recorded by  
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    Abdominal Radiology.2023;[Epub]     CrossRef
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    Wenhua Xu, Hongwu Zhang, Qinfeng Zhang, Jialan Xu
    Environmental Toxicology.2022; 37(3): 637.     CrossRef
  • High Glycated Hemoglobin Instead of High Body Mass Index Might Increase the Urine N-Acetyl-β-D-glucosaminidase Con-Centration in Children and Adolescents with Diabetes Mellitus
    Jin-Soon Suh, Kyoung Soon Cho, Seul Ki Kim, Shin-Hee Kim, Won Kyoung Cho, Min Ho Jung, Moon Bae Ahn
    Life.2022; 12(6): 879.     CrossRef
O-GlcNAc Modification: Friend or Foe in Diabetic Cardiovascular Disease
Udayakumar Karunakaran, Nam Ho Jeoung
Korean Diabetes J. 2010;34(4):211-219.   Published online August 31, 2010
  • 3,478 View
  • 35 Download
  • 16 Crossref
AbstractAbstract PDFPubReader   

O-Linked β-N-acetyl glucosaminylation (O-GlcNAcylation) is a dynamic post-translational modification that occurs on serine and threonine residues of cytosolic and nuclear proteins in all cell types, including those involved in the cardiovascular system. O-GlcNAcylation is thought to act in a manner analogous to protein phosphorylation. O-GlcNAcylation rapidly cycles on/off proteins in a time scale similar to that for phosphorylation/dephosphorylation of proteins. Several studies indicate that O-GlcNAc might induce nuclear localization of some transcription factors and may affect their DNA binding activities. However, at the cellular level, it has been shown that O-GlcNAc levels increase in response to stress and augmentation of this response suppresses cell survival. Increased levels of O-GlcNAc have been implicated as a pathogenic contributor to glucose toxicity and insulin resistance, which are major hallmarks of type 2 diabetes and diabetes-related cardiovascular complications. Thus, O-GlcNAc and its metabolic functions are not yet well-understood; focusing on the role of O-GlcNAc in the cardiovascular system is a viable target for biomedical investigation. In this review, we summarize our current understanding of the role of O-GlcNAc on the regulation of cell function and survival in the cardiovascular system.


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    Tian-Hua Xu, Zitong Sheng, Yue Li, Xiaobo Qiu, Binyao Tian, Li Yao
    Life Sciences.2020; 261: 118121.     CrossRef
  • OGT-Mediated KEAP1 Glycosylation Accelerates NRF2 Degradation Leading to High Phosphate-Induced Vascular Calcification in Chronic Kidney Disease
    Tian-Hua Xu, Yinke Du, Zitong Sheng, Yue Li, Xiaobo Qiu, Binyao Tian, Li Yao
    Frontiers in Physiology.2020;[Epub]     CrossRef
  • The Role of Stress-Induced O-GlcNAc Protein Modification in the Regulation of Membrane Transport
    Viktória Fisi, Attila Miseta, Tamás Nagy
    Oxidative Medicine and Cellular Longevity.2017; 2017: 1.     CrossRef
  • Oral administration of probiotic Lactobacillus paraplantarum BGCG11 attenuates diabetes-induced liver and kidney damage in rats
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    Molecular & Cellular Proteomics.2017; 16(3): 368.     CrossRef
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    Bart Staels
    The American Journal of Medicine.2017; 130(6): S30.     CrossRef
  • Nutrient regulation of transcription and signalling by O-GlcNAcylation
    Gerald W. Hart
    Perspectives in Science.2015; 6: 49.     CrossRef
  • β-Glucan administration to diabetic rats alleviates oxidative stress by lowering hyperglycaemia, decreasing non-enzymatic glycation and protein O-GlcNAcylation
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    Journal of Functional Foods.2013; 5(3): 1226.     CrossRef
  • DecreasedO-GlcNAcylation of the key proteins in kinase and redox signalling pathways is a novel mechanism of the beneficial effect of α-lipoic acid in diabetic liver
    Svetlana Dinić, Jelena Arambašić, Mirjana Mihailović, Aleksandra Uskoković, Nevena Grdović, Jelena Marković, Borivoje Karadžić, Goran Poznanović, Melita Vidaković
    British Journal of Nutrition.2013; 110(3): 401.     CrossRef
  • Modulation of Dynamin-related Protein 1 (DRP1) Function by Increased O-linked-β-N-acetylglucosamine Modification (O-GlcNAc) in Cardiac Myocytes
    Thomas Gawlowski, Jorge Suarez, Brian Scott, Moises Torres-Gonzalez, Hong Wang, Raphaela Schwappacher, Xuemei Han, John R. Yates, Masahiko Hoshijima, Wolfgang Dillmann
    Journal of Biological Chemistry.2012; 287(35): 30024.     CrossRef
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    Diabetes.2011; 60(5): 1399.     CrossRef

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