ArticleHistochemistry and cell biology2015
Over-expression of muscle glycogen synthase in human diabetic nephropathy.
Article in Histochemistry and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Renal glycogen handling in diabetes: A narrative review of diabetic kidney disease pathogenesis.Journal of diabetes investigation · 2026Review
- Small-molecule inhibition of glycogen synthase 1 for the treatment of Pompe disease and other glycogen storage disorders.Science translational medicine · 2024Article
- Effects of experimental ulcerative colitis on myenteric neurons in P2X7-knockout mice.Histochemistry and cell biology · 2023Article
- Ketosis Ameliorates Renal Cyst Growth in Polycystic Kidney Disease.Cell metabolism · 2019Article
- Glucose and glycogen in the diabetic kidney: Heroes or villains?EBioMedicine · 2019Review
- The Antidiabetic Agent Sodium Tungstate Induces Abnormal Glycogen Accumulation in Renal Proximal Tubules from Diabetic IRS2-Knockout Mice.Journal of diabetes research · 2018Article
- Is Type 2 Diabetes a Glycogen Storage Disease of Pancreatic β Cells?Cell metabolism · 2017Review
- The Histochemistry and Cell Biology omnium-gatherum: the year 2015 in review.Histochemistry and cell biology · 2016Review
- Obesity-related insulin resistance: implications for the surgical patient.International journal of obesity (2005) · 2015Review
- In vivo sodium tungstate treatment prevents E-cadherin loss induced by diabetic serum in HK-2 cell line.Journal of cellular physiology · 2015Article
- Preclinical and Clinical Studies for Sodium Tungstate: Application in Humans.Journal of clinical & cellular immunology · 2015Article
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is a major complication of diabetic patients and the leading cause of end-stage renal disease. Glomerular dysfunction plays a critical role in DN, but deterioration of renal function also correlates with tubular alterations. Human DN is characterized by glycogen accumulation in tubules. Although this pathological feature has long been recognized, little information exists about the triggering mechanism. In this study, we detected over-expression of muscle glycogen synthase (MGS) in diabetic human kidney. This enhanced expression suggests the participation of MGS in renal metabolic changes associated with diabetes. HK2 human renal cell line exhibited an intrinsic ability to synthesize glycogen, which was enhanced after over-expression of protein targeting to glycogen. A correlation between increased glycogen amount and cell death was observed. Based on a previous transcriptome study on human diabetic kidney disease, significant differences in the expression of genes involved in glycogen metabolism were analyzed. We propose that glucose, but not insulin, is the main modulator of MGS activity in HK2 cells, suggesting that blood glucose control is the best approach to modulate renal glycogen-induced damage during long-term diabetes.
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