scholarly journals Hexosamine biosynthetic pathway activity in leptin resistant sucrose-drinking rats

2015 ◽  
Vol 138 ◽  
pp. 208-218 ◽  
Author(s):  
Ruth B.S. Harris ◽  
John W. Apolzan
Keyword(s):  
Biosynthetic Pathway ◽  
Hexosamine Biosynthetic Pathway ◽  
Pathway Activity ◽  
Sucrose Drinking

scholarly journals The Hexosamine Biosynthetic Pathway as a Therapeutic Target after Cartilage Trauma: Modification of Chondrocyte Survival and Metabolism by Glucosamine Derivatives and PUGNAc in an Ex Vivo Model

2021 ◽  
Vol 22 (14) ◽  
pp. 7247
Author(s):  
Jana Riegger ◽  
Julia Baumert ◽  
Frank Zaucke ◽  
Rolf E. Brenner
Keyword(s):  
Biosynthetic Pathway ◽  
Ex Vivo ◽  
Type Ii Collagen ◽  
Cartilage Explants ◽  
Uridine Diphosphate ◽  
Cell Protection ◽  
Ex Vivo Model ◽  
Human Cartilage ◽  
Hexosamine Biosynthetic Pathway ◽  
Cellular Processes

The hexosamine biosynthetic pathway (HBP) is essential for the production of uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), the building block of glycosaminoglycans, thus playing a crucial role in cartilage anabolism. Although O-GlcNAcylation represents a protective regulatory mechanism in cellular processes, it has been associated with degenerative diseases, including osteoarthritis (OA). The present study focuses on HBP-related processes as potential therapeutic targets after cartilage trauma. Human cartilage explants were traumatized and treated with GlcNAc or glucosamine sulfate (GS); PUGNAc, an inhibitor of O-GlcNAcase; or azaserine (AZA), an inhibitor of GFAT-1. After 7 days, cell viability and gene expression analysis of anabolic and catabolic markers, as well as HBP-related enzymes, were performed. Moreover, expression of catabolic enzymes and type II collagen (COL2) biosynthesis were determined. Proteoglycan content was assessed after 14 days. Cartilage trauma led to a dysbalanced expression of different HBP-related enzymes, comparable to the situation in highly degenerated tissue. While GlcNAc and PUGNAc resulted in significant cell protection after trauma, only PUGNAc increased COL2 biosynthesis. Moreover, PUGNAc and both glucosamine derivatives had anti-catabolic effects. In contrast, AZA increased catabolic processes. Overall, “fueling” the HBP by means of glucosamine derivatives or inhibition of deglycosylation turned out as cells and chondroprotectives after cartilage trauma.

scholarly journals Hexosamine Biosynthetic Pathway Mutations Cause Neuromuscular Transmission Defect

2011 ◽  
Vol 88 (2) ◽  
pp. 162-172 ◽  
Author(s):  
Jan Senderek ◽  
Juliane S. Müller ◽  
Marina Dusl ◽  
Tim M. Strom ◽  
Velina Guergueltcheva ◽  
...  
Keyword(s):  
Neuromuscular Transmission ◽  
Biosynthetic Pathway ◽  
Hexosamine Biosynthetic Pathway

Hyperglycemia induces PAI-1 gene expression in adipose tissue by activation of the hexosamine biosynthetic pathway

2002 ◽  
Vol 160 (1) ◽  
pp. 115-122 ◽  
Author(s):  
Ilan Gabriely ◽  
Xiao Man Yang ◽  
Jane A Cases ◽  
Xiao Hui Ma ◽  
Luciano Rossetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Biosynthetic Pathway ◽  
Hexosamine Biosynthetic Pathway ◽  
Pai 1

scholarly journals Hexosamine Biosynthetic Pathway Inhibition Leads to AML Cell Differentiation and Cell Death

2018 ◽  
Vol 17 (10) ◽  
pp. 2226-2237 ◽  
Author(s):  
Abhishek Asthana ◽  
Parameswaran Ramakrishnan ◽  
Yorleny Vicioso ◽  
Keman Zhang ◽  
Reshmi Parameswaran
Keyword(s):  
Cell Death ◽  
Cell Differentiation ◽  
Biosynthetic Pathway ◽  
Hexosamine Biosynthetic Pathway ◽  
Pathway Inhibition

Hyperglycemia modulates angiotensinogen gene expression

2001 ◽  
Vol 281 (3) ◽  
pp. R795-R802 ◽  
Author(s):  
Ilan Gabriely ◽  
Xiao Man Yang ◽  
Jane A. Cases ◽  
Xiao Hui Ma ◽  
Luciano Rossetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Biosynthetic Pathway ◽  
Fold Increase ◽  
Suppressive Effect ◽  
Sprague Dawley ◽  
Hexosamine Biosynthetic Pathway ◽  
Obese Rats ◽  
Agt Gene

Elevated plasma angiotensinogen (AGT) levels have been demonstrated in insulin-resistant states such as obesity and type 2 diabetes mellitus (DM2), conditions that are directly correlated to hypertension. We examined whether hyperinsulinemia or hyperglycemia may modulate fat and liver AGT gene expression and whether obesity and insulin resistance are associated with abnormal AGT regulation. In addition, because the hexosamine biosynthetic pathway is considered to function as a biochemical sensor of intracellular nutrient availability, we hypothesized that activation of this pathway would acutely mediate in vivo the induction of AGT gene expression in fat and liver. We studied chronically catheterized lean (∼300 g) and obese (∼450 g) Sprague-Dawley rats in four clamp studies ( n= 3/group), creating physiological hyperinsulinemia (∼60 μU/ml, by an insulin clamp), hyperglycemia (∼18 mM, by a pancreatic clamp using somatostatin to prevent endogenous insulin secretion), or euglycemia with glucosamine infusion (GlcN; 30 μmol · kg−1 · min−1) and equivalent saline infusions (as a control). Although insulin infusion suppressed AGT gene expression in fat and liver of lean rats, the obese rats demonstrated resistance to this effect of insulin. In contrast, hyperglycemia at basal insulin levels activated AGT gene expression in fat and liver by approximately threefold in both lean and obese rats ( P < 0.001). Finally, GlcN infusion simulated the effects of hyperglycemia on fat and liver AGT gene expression (2-fold increase, P < 0.001). Our results support the hypothesis that physiological nutrient “pulses” may acutely induce AGT gene expression in both adipose tissue and liver through the activation of the hexosamine biosynthetic pathway. Resistance to the suppressive effect of insulin on AGT expression in obese rats may potentiate the effect of nutrients on AGT gene expression. We propose that increased AGT gene expression and possibly its production may provide another link between obesity/insulin resistance and hypertension.

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