Guide Glycolysis and it’s positive effects on osteoblast activity | WNT3A/10B

[Mandy?]

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

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!

 

[Mandy?]

Tags tbh: @Currycelloser @Marlonmogsyouhaha @draftLexy ,and cause I feel nice, @Newday

 

[Marlonmogsyouhaha]

Here to save the looksmaxxing section

 

[LaWi]

Mirin effort

 

[Mandy?]

@999. New ting ting thread

 

[999.]

@999. New ting ting thread

mirin

 

[Mandy?]

No traction it’s so over

 

[Currycelloser]

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
View attachment 308712
View attachment 308713

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.
View attachment 308719
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



View attachment 308730
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.



View attachment 308744
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.







View attachment 308753
View attachment 308755
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!

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
View attachment 308712
View attachment 308713

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.
View attachment 308719
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



View attachment 308730
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.



View attachment 308744
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.







View attachment 308753
View attachment 308755
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!

before working out, eating 15 of glucose powder is enough to stimulate this process without disrupting u from ketosis, and u dont need more than 15 of glucose and it doesnt lead to significant increase in bonemass and strength via this pathway

 

[Mandy?]

before working out, eating 15 of glucose powder is enough to stimulate this process without disrupting u from ketosis, and u dont need more than 15 of glucose and it doesnt lead to significant increase in bonemass and strength via this pathway

Why exactly 15g?

 

[Currycelloser]

Why exactly 15g?

cause above 15 g negative effects of glucose starts also, advanced glycation end products seems to inhibit bone growth, and increasig dietary uptake of glucose doesnt lead to more bone growth stimulus via this pathway

 

[Mandy?]

cause above 15 g negative effects of glucose starts also, advanced glycation end products seems to inhibit bone growth, and increasig dietary uptake of glucose doesnt lead to more bone growth stimulus via this pathway

Advanced glycation products do not happen,even with 300g carbs daily. If you would you know already,AGEs are largely triggered by free amino acids and hyperglycemia.

 

[Mandy?]

cause above 15 g negative effects of glucose starts also, advanced glycation end products seems to inhibit bone growth, and increasig dietary uptake of glucose doesnt lead to more bone growth stimulus via this pathway

Advanced glycation products do not happen,even with 300g carbs daily. If you would you know already,AGEs are largely triggered by free amino acids and hyperglycemia.

Imagine also thinking 15g of carbs is enough to fuel even 10% of your whole body.

 

[Currycelloser]

Advanced glycation products do not happen,even with 300g carbs daily. If you would you know already,AGEs are largely triggered by free amino acids and hyperglycemia.

AGEs are triggered by free amino acids binding to glucose, and saying 300g of carbs doesnt seem to increase AGEs is false biochemically, and chronic upregulation of insulin via dietary glucose increases AGEs

 

[Mandy?]

AGEs are triggered by free amino acids binding to glucose, and saying 300g of carbs doesnt seem to increase AGEs is false biochemically, and chronic upregulation of insulin via dietary glucose increases AGEs

Chronic glucose uptake without insulin reponse=hyperglycemia
You can still consume 300g of carbohydrates without constantly causing insulin release,and it really boils down to how efficient GLUT4 vessels transport glucose.

 

[Mandy?]

AGEs are triggered by free amino acids binding to glucose, and saying 300g of carbs doesnt seem to increase AGEs is false biochemically, and chronic upregulation of insulin via dietary glucose increases AGEs

Chronic glucose uptake without insulin response=hyperglycemia
You can still consume 300g of carbohydrates without constantly causing insulin release,and it really boils down to how efficient GLUT4 vessels transport glucose.

Hyperglycemia is also merely factored of how your liver clears it’s glycogen and how well insulin reponses,which is not directly just caused by carbohydrate intake.

 

[Currycelloser]

Imagine also thinking 15g of carbs is enough to fuel even 10% of your whole body.

gluconeogenesis works for lots of functions btw

 

[Currycelloser]

Chronic glucose uptake without insulin reponse=hyperglycemia
You can still consume 300g of carbohydrates without constantly causing insulin release,and it really boils down to how efficient GLUT4 vessels transport glucose.

huh? carbs are the primary reason for spiking of insulin, even 10g of dietary carbs raise insulin no matter how healthy u are, and constant upregulation if insulin throughout the day is bad

 

[Mandy?]

gluconeogenesis works for lots of functions btw

FaceIQ ahh argument,inferior energy production and is very demanding rather than exogenous glucose.

huh? carbs are the primary reason for spiking of insulin, even 10g of dietary carbs raise insulin no matter how healthy u are, and constant upregulation if insulin throughout the day is bad

Yes,but hyperglycemia is mostly caused by poor insulin response,glucose duration in bloodstream,liver glycogen etc. insulin resistance is not even caused by the glucose molecule itself,it’s hundreds of factors,saying glucose is the main factor is like “30 guys are punching me,but only 1 carries the fault.”

 

[Mandy?]

huh? carbs are the primary reason for spiking of insulin, even 10g of dietary carbs raise insulin no matter how healthy u are, and constant upregulation if insulin throughout the day is bad

Literal linear thinking of you if you think “glucose->insulin response->insulin resistance and AGEs”

 

[Currycelloser]

FaceIQ ahh argument,inferior energy production and is very demanding rather than exogenous glucose.

proof?

Yes,but hyperglycemia is mostly caused by poor insulin response,glucose duration in bloodstream,liver glycogen etc. insulin resistance is not even caused by the glucose molecule itself,it’s hundreds of factors,saying glucose is the main factor is like “30 guys are punching me,but only 1 carries the fault.”

sure i agree with that, we dont know the causal inference of insulin resistance and there are multiple factors

Literal linear thinking of you if you think “glucose->insulin response->insulin resistance and AGEs”

huh? i never said glucose cause insulin resistance?? U said glucose uptake doesnt raise insulin always which is untrue, no matter how healthy u are, glucose cause insulin spikes and 300g of carbs, will 100% cause AGEs as it will combine with free amino acids. If u eat 300g of carbs in one meal it causes a very high insulin spike which makes u nausious but even if u split 300g of carbs multiple times a day, u will get chronic upregulation of insulin throughout the day which is still bad