ArticleFrontiers in nutrition2022
Glucosamine inhibits extracellular matrix accumulation in experimental diabetic nephropathy.
Article in Frontiers in nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Tibia length is an appropriate standard for evaluating hypertrophy in streptozotocin-induced diabetic complications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bushen Tongluo recipe improves oxidative stress homeostasis, inhibits transforming growth factor/Notch signaling pathway, and regulates the lncRNA maternally expressed gene 3/miR-145 axis to delay diabetic kidney disease.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Upregulation of Piezo2 and increased extracellular matrix protein in diabetic kidney disease mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Mizagliflozin ameliorates diabetes induced kidney injury by inhibitor inhibit inflammation and oxidative stress.World journal of diabetes · 2025Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
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Abstract
Introduction: Glucosamine, the intermediate metabolite of the hexosamine biosynthesis pathway (HBP), is widely used as a supplementary drug in patients with osteoarthritis. However, its consequences in such patients concomitantly suffering from diabetic nephropathy is unknown. Methods: The aim of the study was to investigate the effect of exogenous administration of glucosamine in the diabetic kidney. A mouse model of streptozotocin-induced diabetic nephropathy Results: There was no significant difference in urinary albumin secretion, relative kidney weight, or creatinine clearance between the groups treated with glucosamine and controls. Assessment of the kidney demonstrated reduction in mesangial expansion and fibronectin expression in the diabetic glomeruli treated with glucosamine. Glucosamine treatment significantly decreased α-smooth muscle actin (α-SMA) protein expression in both diabetic and control kidneys, whereas the expression of other fibrosis-related genes and inflammatory factors was unaltered. Moreover, α-SMA colocalized with the endothelial marker CD31 in the diabetic and control kidneys, and glucosamine reduced α-SMA+ ECs in the diabetic glomeruli. In addition, glucosamine suppressed α-SMA expression in endothelial cells treated with or without high glucose. Discussion: In summary, this is the first report to show that glucosamine reduces mesangial expansion and inhibits endothelial-mesenchymal transition in diabetic nephropathy. The underlying mechanisms need to be further investigated.
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