CR mimicry with glucose mimics
treonsverdery
22 Feb 2009
I was thinking that chemicals that mimic glucose yet jump off the various pathways would confer longevity like CR Further I thought that different glucose mimetics would act on different pathways thus giving knowledge about different pathways of CR juvenation
My thoughts were halogenated glucose (tight fit monopolization) as well as superdeuterated (heavy gradual receptor effects) glucose would do CR mimicry Visiting pubmed.org shows CR mimicry with 2Deoxy glucose which is basically regular glucose with a hydrogen atom where an -OH would usually be
http://www.ncbi.nlm.nih.gov/pubmed/19013500?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportP
anel.Pubmed_RVDocSum 2-Deoxy-d-glucose (2DG) is an analog of glucose that is effectively taken up by cells competing with normal glucose but cannot be further utilized to produce energy. It was previously reported that 2DG can mimic the beneficial effects of dietary restriction in experimental models of neurodegenerative disorders and cancer. In the present study, we report that pretreatment with 2DG increases the resistance of neural progenitor cells (NPC) to oxidative insults. 2DG significantly suppressed the proliferation of NPC, and high concentrations of 2DG were toxic to NPC. However, a treatment with a moderate concentration of 2DG protected the NPC against tBHP-induced oxidative stress suggesting that this chemical had hormetic action mimicking dietary restriction. Furthermore, we showed that the protective mechanism of 2DG involved the activation of AMP-activated protein kinase. Our findings demonstrate that 2DG can modulate the cellular responses to oxidative stress and confer cellular resistance in NPC by activating the metabolic regulator.
The opportunity to communicate here is: What are readers drug structures for a super effective CR mimetic Is it more funner to think of a glucose mimetic at the citric acid cycle or as a visitor to specific regulator n cummunication tissues like the pancreas liver or brain If the glucose mimetic is targeted at a cytocommunications center thats very different than being at the citric acid cycle at every cyte as part of ATP generation
Just to make this topic even sexier Think on the way MRI uses glucose utilization to show which brain regions are active Now briefly imagine that different parts of the brain react differently to different glucose mimetics like http://www.ncbi.nlm....Pubmed_RVDocSum Whether neurons act one way glia another or something really far out like the ancient reptilian cortex has different glucose mimetic processing than the neocortex the idea of foods specific to areas of brain anatomy that provide juvenation benefits is Groovy
Edited by treonsverdery, 22 February 2009 - 11:53 PM.
My thoughts were halogenated glucose (tight fit monopolization) as well as superdeuterated (heavy gradual receptor effects) glucose would do CR mimicry Visiting pubmed.org shows CR mimicry with 2Deoxy glucose which is basically regular glucose with a hydrogen atom where an -OH would usually be
http://www.ncbi.nlm.nih.gov/pubmed/19013500?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportP
anel.Pubmed_RVDocSum 2-Deoxy-d-glucose (2DG) is an analog of glucose that is effectively taken up by cells competing with normal glucose but cannot be further utilized to produce energy. It was previously reported that 2DG can mimic the beneficial effects of dietary restriction in experimental models of neurodegenerative disorders and cancer. In the present study, we report that pretreatment with 2DG increases the resistance of neural progenitor cells (NPC) to oxidative insults. 2DG significantly suppressed the proliferation of NPC, and high concentrations of 2DG were toxic to NPC. However, a treatment with a moderate concentration of 2DG protected the NPC against tBHP-induced oxidative stress suggesting that this chemical had hormetic action mimicking dietary restriction. Furthermore, we showed that the protective mechanism of 2DG involved the activation of AMP-activated protein kinase. Our findings demonstrate that 2DG can modulate the cellular responses to oxidative stress and confer cellular resistance in NPC by activating the metabolic regulator.
The opportunity to communicate here is: What are readers drug structures for a super effective CR mimetic Is it more funner to think of a glucose mimetic at the citric acid cycle or as a visitor to specific regulator n cummunication tissues like the pancreas liver or brain If the glucose mimetic is targeted at a cytocommunications center thats very different than being at the citric acid cycle at every cyte as part of ATP generation
Just to make this topic even sexier Think on the way MRI uses glucose utilization to show which brain regions are active Now briefly imagine that different parts of the brain react differently to different glucose mimetics like http://www.ncbi.nlm....Pubmed_RVDocSum Whether neurons act one way glia another or something really far out like the ancient reptilian cortex has different glucose mimetic processing than the neocortex the idea of foods specific to areas of brain anatomy that provide juvenation benefits is Groovy
Edited by treonsverdery, 22 February 2009 - 11:53 PM.
