tyw
Member
As per the title:
This is something most people here should already know -- that availability of fatty acids is the limiting factor to cancer proliferation.
This study in particular used the CPT-1 inhibitor Etomoxir on live mice with the appropriate tumours -- Etomoxir - Wikipedia, the free encyclopedia
Once sufficient numbers of cancerous cells are present, they seem to sustain themselves on anything. (see section 'Metabolic Fuel Requirements of Primary-Cultured Human Glioma Cells')
Once the "cancer progression" has started, inhibiting CPT1 does not prevent further progression -- fatty acid metabolism seems to be a "jump-starter", which once started, the cancerous cells can continue to proliferate without major fatty acid metabolic boosts.
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In real life terms, it is not known if keeping carbohydrate intake high is going to prevent such a scenario.
It is very clear that malonyl-CoA will inhibit CPT1 as well, and this is the primary mode of action for the Randle Effect in particular tissues (eg: the liver). Would maintaining consistent liver glycogen levels prevent such a cascade? No clue.
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Fatty acid oxidation is required for the respiration and proliferation of malignant glioma cells (Hua et. al., 2016)
This is something most people here should already know -- that availability of fatty acids is the limiting factor to cancer proliferation.
This study in particular used the CPT-1 inhibitor Etomoxir on live mice with the appropriate tumours -- Etomoxir - Wikipedia, the free encyclopedia
In this study, we report that cells derived from human glioma and cultured under optimal conditions express fatty acid oxidation enzymes and are dependent upon fatty acid oxidation for aerobic respiration and proliferative activity.
Figure 2 demonstrates that a majority of respiratory activity arises from fatty acid oxidation, while a smaller subset of respiratory activity arises from glucose oxidation. These findings are interesting in light of results in humans and suggest that much of the acetyl-CoA produced by malignant gliomas arises from nonglucose sources
Pretty straightforward -- Fatty acids required for cancer cells to grow. Figure 2 demonstrates that a majority of respiratory activity arises from fatty acid oxidation, while a smaller subset of respiratory activity arises from glucose oxidation. These findings are interesting in light of results in humans and suggest that much of the acetyl-CoA produced by malignant gliomas arises from nonglucose sources
Once sufficient numbers of cancerous cells are present, they seem to sustain themselves on anything. (see section 'Metabolic Fuel Requirements of Primary-Cultured Human Glioma Cells')
Once the "cancer progression" has started, inhibiting CPT1 does not prevent further progression -- fatty acid metabolism seems to be a "jump-starter", which once started, the cancerous cells can continue to proliferate without major fatty acid metabolic boosts.
----
In real life terms, it is not known if keeping carbohydrate intake high is going to prevent such a scenario.
It is very clear that malonyl-CoA will inhibit CPT1 as well, and this is the primary mode of action for the Randle Effect in particular tissues (eg: the liver). Would maintaining consistent liver glycogen levels prevent such a cascade? No clue.
....
