2 edition of Role of the polyol pathway in high glucose-induced altered glomerular mesangial cell function. found in the catalog.
Role of the polyol pathway in high glucose-induced altered glomerular mesangial cell function.
Thesis (M.Sc.) -- University of Toronto, 1995.
|Series||Canadian theses = -- Thèses canadiennes|
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Excess collagen IV expression by mesangial cells contributes to diabetic glomerulosclerosis. We hypothesized that in high glucose reactive oxygen species (ROS) generation by Cited by: This paper focuses on the role that mitogen-activated protein kinases (MAPKs) play in drug-induced kidney injury. The MAPKs, of which there are four major classes (ERK, p38, JNK, and ERK5/BMK), are signalling cascades which have been found to be broadly conserved across a wide variety of organisms. MAPKs allow effective transmission of information from the cell Cited by:
Hence, these cell types are exposed to polyol pathway ac-tivation in diabetes. These are also the cells that manifest the best-known changes or damage in diabetes . The biochemical consequences of polyol pathway activation have been studied in the whole retina of diabetic animals. The best-documented are the accumulation of sorbitol and fruc-. The mesangial cells proliferation Intracellular signaling pathway mediated by the ppRb. The role of autophagy in cellular senescence The molecular mechanisms of the glomerular cell senescence associated with chronic inhibition File Size: KB.
Start studying Function and Structure of the Kidneys. Learn vocabulary, terms, and more with flashcards, games, and other study tools. Diabetic nephropathy (DN) is a serious complication that commonly confronted by diabetic patients. A common theory for the pathogenesis of this renal dysfunction in diabetes is cell injury, inflammation as well as oxidative stress. In this content, the detailed molecular mechanism underlying high glucose induced renal tubular epithelial injury was by:
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High glucose-induced mesangial cell altered contractility: role of the polyol pathway. Derylo B(1), Babazono T, Glogowski E, Kapor-Drezgic J, Hohman T, Whiteside C.
Author information: (1)Department of Medicine and Institute of Medical Science, University of Toronto, by: Therefore, high glucose-induced loss of mesangial cell contractility, diacylglycerol accumulation and altered protein kinase C activity are mediated through activation of the polyol-pathway, although no specific relationship between elevated diacylglycerol and protein kinase C activity was by: The polyol pathway can be active in the human retina; it can be active in endothelial cells and not just in pericytes; it can be the mechanism for the changes we see in the Müller cells of human diabetic retinas; through activity in endothelial and Müller cells the pathway can be a strong contributor to the disturbed fluid homeostasis that occurs in the diabetic retina Cited by: B.
Derylo et al.: High glucose-induced mesangial cell altered contractility phosphoric acid, % T ween 20 and one change of 75 mmol/l sodium phosphate, (pH ). The role of the polyol pathway in promoting oxidative stress in diabetic complications is an active area of investigation.
There is accumulating evidence from preclinical cellular and animal studies indicating that glucose flux through this pathway is the major source of oxidative stress involved in the pathogenesis of diabetic complications, particularly diabetic retinopathy and diabetic nephropathy.
polyol pathway plays a role in mediating the replica- tive abnormalities of human endothelial cells cultured in high glucose and whether these cells accumulate glucose 6-phosphate, which is a most potent effector of nonenzymatic glycosylation [14, 15].
Materials and methods Cell cultureCited by: Polyol pathway plays an important role in the pathogenesis of DM in human patients. Indeed a number of AR inhibitors are currently being investigated to prevent diabetic : Marjorie Dunlop.
The Polyol Pathway. The polyol pathway was the first pathway to be defined linking hyperglycemia to microvascular complications (Brownlee, ; Gabbay, Merola, & Field, ).
Aldose reducatse (AR), the first enzyme in this pathway, has low affinity to glucose at normal concentrations; however, in diabetes, increasing amounts of glucose are converted by AR to.
The polyol pathway is a two-step process that converts glucose to fructose. In this pathway glucose is reduced to sorbitol, which is subsequently oxidized to fructose. It is also called the sorbitol-aldose reductase pathway.
The sorbitol pathway plays a role in diabetic renal complications because aldose reductase metabolizes the excess of glucose to toxic metabolites that induce hyperfiltration and glomerular dysfunction. The SphK1 pathway and FN expression were examined in streptozotocin-induced diabetic rat kidney and glomerular mesangial cells (GMC) exposed to high glucose (HG).
FN up-regulation was concomitant with activation of the SphK1 pathway as reflected in an increase in the expression and activity of SphK1 and sphingosine 1-phosphate (S1P) production in both diabetic kidney and HG-treated Cited by: Polyol Pathway and Role in Diabetes Pathogenesis lesson.
What is the purpose of the Polyol (Sorbitol-Aldose Reductase) Pathway, and what is the role of the p. In addition, in cultured mesangial cells, high glucose-induced DAG accumulation, PKC activation, and TGF-β overproduction were mediated through polyol pathway activation (82, 83).
In cultured proximal tubular cells, PKC and polyol pathway activation mediated the high glucose-induced collagen and fibronectin accumulation by decreasing their Cited by: The polyol pathway is a pathway of glucose metabolism and is regarded as an important element in the pathogenesis of refractive changes, cataract formation and diabetic retinopathy in individuals with diabetes mellitus.
The focus of this review is on the role of the polyol pathway in the pathogenesis of diabetic complications in the eye. Podocytes change the size of the glomerular filtration slits. If the slits widen, more surface area is available for filtration, and GFR increases. Contraction of mesangial cells apparently changes the glomerular capillary surface area available for filtration.
the lipidosis in glomerular endothelial and mesangial cells. To test that, we exposed the cultured glomerular endothelial and mesangial cells to the CM, iomeprol, to evaluate whether this treatment will cause the lipid accu-mulation as we observed in vivo (Additional file 1).
In detail, cells were treated with iomeprol or cultured inAuthor: Hua Su, Chen Ye, Qian Wen, Hong-Yan Zhu, Li-Xia Yi, Chun Zhang. Investigating the Role of the Polyol Pathway in the Central Nervous System The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.
Listing a study does not mean it has been evaluated by the U.S. Federal Government. Search term. Advanced Search Citation Search.
Search term. Second, the intermediate 3‐deoxyglucone is a precursor of AGEs. Thus, activation of the polyol pathway increases oxidative stress and also enhances AGE formation.
Interestingly, recent data suggest that the calcium antagonist amlodipine inhibits sorbitol formation, indicating blockade of the polyol by: Adenosine-induced apoptosis in glomerular mesangial cells ZHIHUI ZHAO,TOROS KAPOIAN,MICHELLE SHEPARD, and ELIAS A.
LIANOS Nephrology Division, Department of Medicine, Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA Adenosine-induced apoptosis in glomerular mesangial cells.
lular or extracellular nucleotides by. A. Ultrastructure and Function of the Glomerulus. As shown by the ultrastructure illustrated in Figure 1, the glomerulus contains capillary networks that allow the filtration of large plasma volumes at the renal entering the glomerulus through afferent arterioles, plasma filters through fenestrated endothelial cells of the glomerular basement membrane (basal Cited by: The physiological role of aldose reductase in the kidney, the rate limiting enzyme of the polyol pathway, is the intracellular accumulation of the osmolyte sorbitol as an important mechanism in the long-term adaptation of the cell to a rise in the extracellular osmolarity (Grunewald and Kinne, ).
High extracellular.Glucose-induced endothelial dysfunction plays a fundamental role in the development of diabetic vascular complications and glycemic control (the foundation of diabetes care) provides limited protection against the cardiovascular complications.
Therefore, identification of novel drug targets and treatment approaches for diabetes complications represent a key direction of current Author: Domokos Gero.