TheOsei
Deathnic Ltn
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Felt nice might delete later
ATP is highly important for cellular function; it can be created either through glycolysis or oxidative phosphorylation (OXPHOS).
OXPHOS makes 32-34 ATP per glucose
Glycolysis merely 2 ATP per glucose
HOWEVER, the epiphyseal growth plates are hypoxic. Due to a lot of HIF‑1α activation, makes chindrocytes survive there.
Cuz there is no oxygen, OXPHOS is not an option, and chondrocytes are highly adapted to rely on glycolysis for energy anyways
So, we can maximize the energy produced from glycolysis by stabilizing PKM2 in its highly active TETRAMERIC state
Usually the body can switch PKM2 to a less active dimeric form under catabolic conditions. This state is shit to cartilage, drives matrix degradation and impairs mitochondrial function.
Also, knockdown of PKM2 severely reduces chondrocyte proliferation and induces apoptosis, along with the downregulation of COL2A1 and SOX‑9
How do you lock PKM2 into its active tetrameric state?
TEPP‑46 is currently the most potent and selective
DASA‑58 is also decent but honestly gets terrad
In conclusion, upregulating PKM2 into a tetrameric state increases glycolytic flux and ATP production, which in turn improves chondrocyte proliferation and matrix synthesis.
TEPP-46 150mg EOD >>
Studies for dweebs:
Dimeric PKM2 in chondrocytes impairs mitochondrial homeostasis in osteoarthritis: https://pubmed.ncbi.nlm.nih.gov/41881976/
Glycolysis is the ideal energy source for growth plate chondrocytes: https://www.nature.com/articles/s41574-024-00969-x
ATP is highly important for cellular function; it can be created either through glycolysis or oxidative phosphorylation (OXPHOS).
OXPHOS makes 32-34 ATP per glucose
Glycolysis merely 2 ATP per glucose
HOWEVER, the epiphyseal growth plates are hypoxic. Due to a lot of HIF‑1α activation, makes chindrocytes survive there.
Cuz there is no oxygen, OXPHOS is not an option, and chondrocytes are highly adapted to rely on glycolysis for energy anyways
So, we can maximize the energy produced from glycolysis by stabilizing PKM2 in its highly active TETRAMERIC state
Usually the body can switch PKM2 to a less active dimeric form under catabolic conditions. This state is shit to cartilage, drives matrix degradation and impairs mitochondrial function.
Also, knockdown of PKM2 severely reduces chondrocyte proliferation and induces apoptosis, along with the downregulation of COL2A1 and SOX‑9
How do you lock PKM2 into its active tetrameric state?
TEPP‑46 is currently the most potent and selective
DASA‑58 is also decent but honestly gets terrad
In conclusion, upregulating PKM2 into a tetrameric state increases glycolytic flux and ATP production, which in turn improves chondrocyte proliferation and matrix synthesis.
TEPP-46 150mg EOD >>
Studies for dweebs:
Dimeric PKM2 in chondrocytes impairs mitochondrial homeostasis in osteoarthritis: https://pubmed.ncbi.nlm.nih.gov/41881976/
Glycolysis is the ideal energy source for growth plate chondrocytes: https://www.nature.com/articles/s41574-024-00969-x
