hexosamine


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hexosamine

[hek′säs·ə‚mēn]
(biochemistry)
A primary amine derived from a hexose by replacing the hydroxyl with an amine group.
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17] In addition, previous studies showed that high levels of glucose can promote hexosamine biosynthetic pathways and lead to the formation of excess GlcNAc and an increase of O-GlcNAc modifications.
Hyperglycemia is known to activate the various metabolic pathways ([1]) including diacylglycerol (DAG)-protein Kinase C (PKC) pathway, hexosamine pathway, polyol pathway, advanced glycation endproducts (AGE) pathway, and many more, which leads to both acute and chronic inflammatory cascades, resulting in oxidative stress, depending on the type of stimulus, i.
The major metabolic changes occurring at the cellular level are: increased aldose reductase activity (polyol-sorbitol pathway], diacylglycerol--protein kinase C activation [6] (myo-inositol pathway], the hexosamine activation pathway and formation of advanced glycation end products (AGEs].
Studies show that the endoplasmic reticulum (a type of organelle that plays an important role in transporting sugars and proteins across the cell membrane) and the hexosamine pathway, which I described earlier in this article, are involved in apoptosis.
Hexosamine biosynthesis pathway and O-GlcNAcylation have important functions in pig pre-implantation embryonic development and that inhibition of O-GlcNAcase is fatal for development [7].
Suboptimal MnSOD related to insufficient levels of manganese could result in increased mitochondrial ROS formation, which may directly cause macromolecular damage or might indirectly result in oxidative stress by activating stress-sensitive pathways such as the NFkB, p38 MAPK, JNK/SPAK, and hexosamine pathways (Evans et al.
Mediated by the hexosamine pathway, glucose is converted to uridine 5'-diphospho-N-acetylhexosamine (UDP-GNAc), which is subsequently synthesized to glycoproteins, proteoglycans, and glycolipids (Lau & Dennis 2008).
There are other possible described mechanisms, such as increased sorbitol formation through the polyol pathway [2,4], increased protein-kinase C activation [1,2,5], and the hexosamine pathway [2].
The hyperglycaemia in diabetic complications could be explained by increased production of reactive oxygen species (ROS) through the polyol pathway flux, increased formation of advanced glycationend-products (AGEs), increased expression of the receptor for AGEs, activation of protein kinase C isoforms, and over-activity of the hexosamine pathway.
In a forward genetic screen, I found a link between metabolites in the hexosamine pathway and cellular protein quality control.
polyolpathways, hexosamine pathway, protein kinase C and advanced glycosylation end-products which cause hyperglycemia27,28.
Hexosamine, being the important constituents of mucopolysaccharide, is essential component of granulation tissue.