Relevant bibliographies by topics / Diabetic nephropathy; Polyol pathway; Hyperglycaemia

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Diabetic nephropathy; Polyol pathway; Hyperglycaemia'

Author: Grafiati
Published: 5 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Diabetic nephropathy; Polyol pathway; Hyperglycaemia"

1

Thaifa, M.S, Kumar Manoj, U.S Arya, and G. Babu Aparna. "Diabetic Nephropathy: A Plant Based Approach." Endocrinology & Metabolic Syndrome 10, no. 6 (2021): 3. https://doi.org/10.5281/zenodo.10362117.

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Diabetic nephropathy is a complication associated with diabetes mellitus. Diabetes mellitus is a chronic metabolic disorder caused by impaired metabolism of carbohydrate, fats, proteins resulting in hyperglycaemia leading to decreased utilization of carbohydrate, excessive glycogenolysis and gluconeogenesis from amino acids and fatty acids. Diabetic nephropathy is a kidney disease induced by diabetes and occurs due to high blood sugar in the kidney. Keywords: Diabetic nephropathy; Polyol pathway; Hyperglycaemia
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Wada, Jun, and Hirofumi Makino. "Inflammation and the pathogenesis of diabetic nephropathy." Clinical Science 124, no. 3 (2012): 139–52. http://dx.doi.org/10.1042/cs20120198.

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The most problematic issue in clinical nephrology is the relentless and progressive increase in patients with ESRD (end-stage renal disease) worldwide. The impact of diabetic nephropathy on the increasing population with CKD (chronic kidney disease) and ESRD is enormous. Three major pathways showing abnormality of intracellular metabolism have been identified in the development of diabetic nephropathy: (i) the activation of polyol and PKC (protein kinase C) pathways; (ii) the formation of advanced glycation end-products; and (iii) intraglomerular hypertension induced by glomerular hyperfiltrat
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Pisoschi, Catalina, Virgil Darie, and Mihai Serban. "STUDY OF RENAL SORBITOLDEHYDROGENASE IN EXPERIMENTAL DIABETIC NEPHROPATHY." SOUTHERN BRAZILIAN JOURNAL OF CHEMISTRY 6, no. 7 (1998): 77–82. http://dx.doi.org/10.48141/sbjchem.v6.n7.1998.76_1998_2.pdf.

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The link between the polyol pathway and the ocular complications of diabetes mellitus is explained by the excessive storage of sorbitol and the release of osmotic stress. The renal complications could also be explained by the osmotic hypothesis, but the polyol pathway activity is reduced in this case. The study of sorbitol dehydrogenase (SDH) activity, one of the enzymes involved in the catabolism of glucose by this pathway in renal and hepatic homogenates from diabetic animals, shows a constant increase of the hepatic enzyme activity compared to that at the renal level. The different variatio
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Zhang, Yunfang, Junxia Feng, Qi Wang, et al. "Hyperglycaemia Stress-Induced Renal Injury is Caused by Extensive Mitochondrial Fragmentation, Attenuated MKP1 Signalling, and Activated JNK-CaMKII-Fis1 Biological Axis." Cellular Physiology and Biochemistry 51, no. 4 (2018): 1778–98. http://dx.doi.org/10.1159/000495681.

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Background/Aims: Hyperglycaemia stress-induced renal injury is closely associated with mitochondrial dysfunction through poorly understood mechanisms. The aim of our study is to explore the upstream trigger and the downstream effector driving diabetic nephropathy via modulating mitochondrial homeostasis. Methods: A diabetic nephropathy model was generated in wild-type (WT) mice and MAP Kinase phosphatase 1 transgenic (MKP1-TG) mice using STZ injection. Cell experiments were conducted via high-glucose treatment in the human renal mesangial cell line (HRMC). MKP1 overexpression assay was carried
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Kuklin, V. N., J. Matri, N. P. Barlow, et al. "Current trends in management of hyperglycaemia in surgical patients with diabetes mellitus: a review." Annals of critical care, no. 4 (2021): 33–47. http://dx.doi.org/10.21320/1818-474x-2021-4-33-47.

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A large amount of clinical evidences demonstrates a clear association between long-term and/or stress-related hyperglycaemia, and development of complications after surgery. The incidences of perioperative hyperglycaemia are demonstrated in 20-80 % of all cases depending on the type of elective surgery, with the h ighest rate registered in cardiac surgery. The most studied pathophysiological complications of long-term hyperglycaemia in Diabetes Mellitus (DM) patients are; activation of the polyol pathway, diacylglycerol/protein kinase C and hexosamine pathways, advanced glycation product forma
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Tsugawa, T., R. Shinohara, A. Nagasaka, et al. "Alteration of urinary sorbitol excretion in WBN-kob diabetic rats - treatment with an aldose reductase inhibitor." Journal of Endocrinology 181, no. 3 (2004): 429–35. http://dx.doi.org/10.1677/joe.0.1810429.

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An accelerated polyol pathway in diabetes contributes to the development of diabetic complications. To elucidate diabetic nephropathy involving also renal tubular damage, we measured urinary sorbitol concentration concomitantly with urinary N-acetyl-D-glucosaminidase (NAG) excretion in WBN-kob diabetic rats.Twenty-four-hour urinary sorbitol concentrations increased in the diabetic rats in parallel with whole blood sorbitol concentrations. An increase in 24-h urinary NAG excretion coincided with the elevated urinary sorbitol levels in the diabetic rats. The administration of epalrestat, an aldo
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7

Isermann, Berend H., Hongjie Wang, Peter P. Nawroth, and Thati Madhusudhan. "Activated Protein C Targets PI3K-p85/XBP1 Pathway to Inhibit Hyperglycemia Induced Endoplasmic Reticulum Stress in Diabetic Nephropathy." Blood 120, no. 21 (2012): 3354. http://dx.doi.org/10.1182/blood.v120.21.3354.3354.

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Abstract Abstract 3354 Diabetic nephropathy (DN) is a multifactorial disease associated with substantial changes in the haemostatic system. A hallmark of diabetes induced haemostatic dysfunction is impaired thrombomodulin (TM) dependent-protein C (PC) activation. Impaired PC activation triggers glomerular podocyte and endothelial cell dysfunction, thus promoting DN. The intracellular mechanism through which loss of TM and PC activation contributes to DN is not known. Here we show that the haemostatic mediator activated PC (aPC) regulates cellular homeostasis by inhibiting hyperglycemia induced
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Dunlop, Marjorie. "Aldose reductase and the role of the polyol pathway in diabetic nephropathy." Kidney International 58 (September 2000): S3—S12. http://dx.doi.org/10.1046/j.1523-1755.2000.07702.x.

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9

Tarr, Joanna M., Kirti Kaul, Mohit Chopra, Eva M. Kohner, and Rakesh Chibber. "Pathophysiology of Diabetic Retinopathy." ISRN Ophthalmology 2013 (January 15, 2013): 1–13. http://dx.doi.org/10.1155/2013/343560.

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Diabetes is now regarded as an epidemic, with the population of patients expected to rise to 380 million by 2025. Tragically, this will lead to approximately 4 million people around the world losing their sight from diabetic retinopathy, the leading cause of blindness in patients aged 20 to 74 years. The risk of development and progression of diabetic retinopathy is closely associated with the type and duration of diabetes, blood glucose, blood pressure, and possibly lipids. Although landmark cross-sectional studies have confirmed the strong relationship between chronic hyperglycaemia and the
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Marrero, Mario B., Amy K. Banes-Berceli, David M. Stern, and Douglas C. Eaton. "Role of the JAK/STAT signaling pathway in diabetic nephropathy." American Journal of Physiology-Renal Physiology 290, no. 4 (2006): F762—F768. http://dx.doi.org/10.1152/ajprenal.00181.2005.

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Excessive cellular growth is a major contributor to pathological changes associated with diabetic nephropathy. In particular, high glucose-induced growth of glomerular mesangial cells is a characteristic feature of diabetes-induced renal complications. Glomerular mesangial cells respond to traditional growth factors, although in diabetes this occurs in the context of an environment enriched in both circulating vasoactive mediators and high glucose. For example, the vasoactive peptide ANG II has been implicated in the pathogenesis of diabetic renal disease, and recent findings suggest that high
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Dissertations / Theses on the topic "Diabetic nephropathy; Polyol pathway; Hyperglycaemia"

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Palm, Fredrik. "Diabetes-induced Alterations in Renal Microcirculation and Metabolism." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4285.

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Book chapters on the topic "Diabetic nephropathy; Polyol pathway; Hyperglycaemia"

1

Aggarwal, Neerja, and Pawan Kumar Kare. "Diabetes Microvascular Complications: An Overview of Epigenetic Modifications." In Type 2 Diabetes [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94642.

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Diabetic nephropathy (DN) and diabetic retinopathy (DR) are two serious and long-standing microvascular complications of type 2 diabetes mellitus (T2DM) whose burden is increasing worldwide due to increasing burden of T2DM. Several factors which may predispose to the development of DN and DR are persistent hyperglycemia and its consequences such as formation of advanced glycation end products (AGEs), activation of hexosamine pathway, polyol pathway, uncontrolled blood pressure, increased oxidative stress, age, family history of kidney disease or hypertension, ethnic background etc. However, the pathophysiological mechanisms of these complications are complicated and not completely understood yet. Hence it is the demand to discover newer approaches to treat these devastating complications completely. Recently, various epigenetic modifications, which are the transmissible alterations in the expressions of a gene, are being studied to understand the pathophysiology of diabetic vascular complications. Metabolic and environmental factors may lead to dysregulated epigenetic mechanisms which might further affect the chromatin structure and related expressions of a gene, which may lead to diabetes-associated complications. Therefore, it is the need to explore its role in vascular complications in the current scenario. In this chapter, various epigenetic studies with regard to DN and DR, epigenome-wide association studies (EWAS) approach, and starting clinical material for such studies have been discussed. We have also summarized the better understanding of epigenetic alterations and their role in microvascular complications of diabetes through this chapter. The better understanding of epigenetic mechanisms and their role in diabetic microvascular complications could be used in clinical management of DN as well as DR or could be helpful to improve the available therapies for these complications.
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