FoundMyFitness · 2017-07-31 · Rhonda Patrick (host), Guido Kroemer
Dr. Guido Kroemer on Autophagy, Caloric Restriction Mimetics, Fasting & Protein Acetylation
40 claims checked against research: 1 contradicted 2 overstated 3 needing context 30 supported 4 unverified
4 No source found (not proven false)
Acetyltransferases have a low affinity for acetyl-CoA compared to kinases' affinity for ATP, making protein acetylation highly sensitive to fluctuations in acetyl-CoA levels whereas phosphorylation is relatively insensitive to ATP fluctuations.
"acetyltransferases are having a low affinity for acetyl-CoA as compared to kinases, which have a high affinity for ATP. So if you vary the ATP concentration in the cell, it has little impact on phosphorylation reactions. But if you vary acetyl concentration, it has a major impact on the acetylation level of cellular proteins." (said at 0:07:15)
No published record matching the claim that acetyltransferases have a lower affinity for acetyl-CoA compared to kinases' affinity for ATP—rendering protein acetylation sensitive to acetyl-CoA fluctuations while phosphorylation remains relatively insensitive to ATP fluctuations—was located; this does not prove the claim false.
Autophagy can be pharmacologically induced via a cell-permeable Beclin-1-activating peptide or via mTOR inhibitors without inducing protein deacetylation.
"when you induce autophagy by pharmacological tricks such as a cell-permeable peptide that dissociates an inhibitory interaction between a Golgi protein and Beclin-1, you can induce autophagy without that protein deacetylation would occur before. And similarly, when you give chemical inhibitors of mTOR like rapamycin or the rapalogs, there's also no protein deacetylation." (said at 0:11:53)
No published record matching the claim that autophagy can be pharmacologically induced via a cell-permeable Beclin-1-activating peptide or via mTOR inhibitors without inducing protein deacetylation was located; this does not prove the claim false.
In humans, fasting for 3 to 4 days is required to observe robust induction of autophagy in circulating leukocytes.
"what we did on circulating leukocytes is that we needed to wait for 3 or 4 days to see massive induction of autophagy." (said at 0:17:50)
No published record matching the specific claim that 3 to 4 days of fasting is required to observe robust or massive induction of autophagy in human circulating leukocytes was located; this does not prove the claim false. While shorter-term fasting and exercise-induced fasting protocols have been studied for their effects on autophagic markers in human tissues and peripheral blood mononuclear cells, specific empirical publications defining a strict 3- to 4-day requirement for leukocyte autophagy induction were not identified in the indexed literature.
Combining an acetyltransferase inhibitor and a deacetylase activator produces a synergistic effect on autophagy in mice.
"inhibiting the acetyltransferase and activating the deacetylase will have, of course, a synergistic effect. ... Well, you can show this in mice" (said at 0:59:51)
No published record matching the claim that combining an acetyltransferase inhibitor and a deacetylase activator produces a synergistic effect on autophagy in mice was located; this does not prove the claim false.
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.