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Glycolysis and glucose metabolism in osteoblasts, by Mandy.
Hey baby,missed me? Probably not because 70% of the users here weren’t there before I was banned.
But it’s no issue,Mandy is back to teach you more!
What is the WNT3A/WNT10B pathway,how does glucose interact with it?
There’s not much to explain in such a matter,the WNT pathway is a growth pathway,that is the upstream pathway ß-catenin is produced
pubmed.ncbi.nlm.nih.gov
Now instead of simple words like saying “WNT-10b increases bone mass and is stimulated by glucose” etc,we have to look at how it actually interacts in a osteoblastic cell.
I circled 2 areas here,one being the obvious WNT3A/WNT10b pathway,and the other being the GLUT4,1 & 3 pathways.
By the arrow (downstream effect) underneath the marked circle,there is the product of ß-catenin which I already mentioned before. ß-catenin is simple to understand if you follow the arrows,but it directly influences glycolysis
In this example here,which I like more because it shows how much glucose interacts with other pathways such as simple GLUT1 and GLUT4 interacts. Glycolysis is a direct effect that is not only influenced by the WNT10b signal,but also the IGF-1 signals that promote essential anabolism which is shown in the green circle and the insulin binding that is responsible for GLUT4. PDK1 and GLUT4 work synergistically in the TCA cycle,GLUT1 also effects AMPK indirectly by upregulating the ATP/ADP ratio.
I don’t know if you’ll be able to properly read this chart,but I’ll just tell you it’s differences in glucose availability that directly affects osteoblast activity.
Glucose is the primary fuel for osteoblasts,unlike certain tissue that switches between glycolysis and fat oxidation depending on demand,for example muscle that demands glucose upon high intensity cell activity: Osteoblasts are active all the time and are energy demanding,unlike muscle fibers that switch between types (Type I,Type IIa,Type IIx) in order to produce the certain amount of ATP that is set on demand.
this is why most ketocels like facelowIQ and rawmarcus have no dimorphism,their osteoblasts are simply sluggish.
Never go on a keto diet.
I hope you liked my guide,my bad for the formatting. Hopefully you learned something new,if you’re keto then specifically learn from this. Mandy out!
Hey baby,missed me? Probably not because 70% of the users here weren’t there before I was banned.
But it’s no issue,Mandy is back to teach you more!
What is the WNT3A/WNT10B pathway,how does glucose interact with it?
There’s not much to explain in such a matter,the WNT pathway is a growth pathway,that is the upstream pathway ß-catenin is produced
Regulation of osteoblastogenesis and bone mass by Wnt10b - PubMed
Wnts comprise a family of secreted signaling proteins that regulate diverse developmental processes. Activation of Wnt signaling by Wnt10b inhibits differentiation of preadipocytes and blocks adipose tissue development; however, the effect of Wnt10b on other mesenchymal lineages has not been...
pubmed.ncbi.nlm.nih.gov
Now instead of simple words like saying “WNT-10b increases bone mass and is stimulated by glucose” etc,we have to look at how it actually interacts in a osteoblastic cell.
I circled 2 areas here,one being the obvious WNT3A/WNT10b pathway,and the other being the GLUT4,1 & 3 pathways.
By the arrow (downstream effect) underneath the marked circle,there is the product of ß-catenin which I already mentioned before. ß-catenin is simple to understand if you follow the arrows,but it directly influences glycolysis
In this example here,which I like more because it shows how much glucose interacts with other pathways such as simple GLUT1 and GLUT4 interacts. Glycolysis is a direct effect that is not only influenced by the WNT10b signal,but also the IGF-1 signals that promote essential anabolism which is shown in the green circle and the insulin binding that is responsible for GLUT4. PDK1 and GLUT4 work synergistically in the TCA cycle,GLUT1 also effects AMPK indirectly by upregulating the ATP/ADP ratio.
I don’t know if you’ll be able to properly read this chart,but I’ll just tell you it’s differences in glucose availability that directly affects osteoblast activity.
Glucose is the primary fuel for osteoblasts,unlike certain tissue that switches between glycolysis and fat oxidation depending on demand,for example muscle that demands glucose upon high intensity cell activity: Osteoblasts are active all the time and are energy demanding,unlike muscle fibers that switch between types (Type I,Type IIa,Type IIx) in order to produce the certain amount of ATP that is set on demand.
this is why most ketocels like facelowIQ and rawmarcus have no dimorphism,their osteoblasts are simply sluggish.
Never go on a keto diet.
I hope you liked my guide,my bad for the formatting. Hopefully you learned something new,if you’re keto then specifically learn from this. Mandy out!
