S
slinkyfox
Member
- Jun 13, 2012
- 15
- 1
https://en.wikipedia.org/wiki/Oxidative_phosphorylation
https://en.wikipedia.org/wiki/Citric_acid_cycle
http://www.ncbi.nlm.nih.gov/pubmed/26010875 " Studies From Proton Decay"
That last study is way cool... but why would DNP lead to inhibition of mTOR? Caloric deficits lead to inhibition of the EXACT same pathways; reason being your body doesn't want to waste energy on undesired processes such as building bigger muscles. How do you overcome this? Increase calories, generate periods in which insulin is LOUD! . I personally toggle DNP, larger doses on days with caloric deficit and lower doses on lift days. I ensure I am well feed on lift days and this helps me overcome the inhibition caused by a reduction of nutrient availability (essentially what DNP doing). The below study shows... replenishment of ATP levels lead to the reversal of inhibition.
Actions of insulin in fat cells. Effects of low temperature, uncouplers of oxidative phosphorylation, and respiratory inhibitors.
T Kono
Abstract
When isolated rat epididymal fat cells were incubated with [125I]iodoinsulin for 5 min at 37 degrees, radioactivity accumulated in the plasma membrane fraction (Peak 1) and an unidentified particulate fraction (Peak 2) as reported previously (Kono, T., Robinson, F.W., and Sarver, J.A. (1975) J. Biol. Chem. 250, 7826-7835). This accumulation of radioactivity in Peak 2 (but not that in Peak 1) was greatly impaired when cells were incubated with iodoinsulin in the presence of a variety of metabolic inhibitors that reduce the cellular content of ATP. The reduction in the ATP level coincided with a disappearance of the stimulatory effects of insulin on sugar transport and the hormone-sensitive phosphodiesterase. In contrast, ATP depletion had no significant effects, at least during a 5-to 15-min incubation, on the intracellular water space and on the basal sugar transport and phosphodiesterase activities. When cells once depleted on ATP by treatment with 2,4-dinitrophenol (1 mM; 10 min) were washed and suspended in fresh buffer, the ATP level was recovered almost fully in 10 min. This recovery coincided with the restoration of responsiveness to insulin. When cells were incubated with [125I]iodoinsulin or insulin for 5 min at 15 degrees instead of 37 degrees, a negligible quantity of radioactivity accumulated in Peak 2 and insulin failed to activate sugar transport. In contrast, under the same conditions, radioactivity accumulated in Peak 1 and insulin stimulated phosphodiesterase considerably. These results suggest that ATP, or some other compound metabolically related to ATP, may be necessary for the actions of insulin on sugar transport and phosphodiesterase. ATP, or some other related compound, may also be necessary in the formation of the radioactive Peak 2, although the physiological function and cellular location of this peak are yet to be ascertained.
https://en.wikipedia.org/wiki/Citric_acid_cycle
http://www.ncbi.nlm.nih.gov/pubmed/26010875 " Studies From Proton Decay"
That last study is way cool... but why would DNP lead to inhibition of mTOR? Caloric deficits lead to inhibition of the EXACT same pathways; reason being your body doesn't want to waste energy on undesired processes such as building bigger muscles. How do you overcome this? Increase calories, generate periods in which insulin is LOUD! . I personally toggle DNP, larger doses on days with caloric deficit and lower doses on lift days. I ensure I am well feed on lift days and this helps me overcome the inhibition caused by a reduction of nutrient availability (essentially what DNP doing). The below study shows... replenishment of ATP levels lead to the reversal of inhibition.
Actions of insulin in fat cells. Effects of low temperature, uncouplers of oxidative phosphorylation, and respiratory inhibitors.
T Kono
Abstract
When isolated rat epididymal fat cells were incubated with [125I]iodoinsulin for 5 min at 37 degrees, radioactivity accumulated in the plasma membrane fraction (Peak 1) and an unidentified particulate fraction (Peak 2) as reported previously (Kono, T., Robinson, F.W., and Sarver, J.A. (1975) J. Biol. Chem. 250, 7826-7835). This accumulation of radioactivity in Peak 2 (but not that in Peak 1) was greatly impaired when cells were incubated with iodoinsulin in the presence of a variety of metabolic inhibitors that reduce the cellular content of ATP. The reduction in the ATP level coincided with a disappearance of the stimulatory effects of insulin on sugar transport and the hormone-sensitive phosphodiesterase. In contrast, ATP depletion had no significant effects, at least during a 5-to 15-min incubation, on the intracellular water space and on the basal sugar transport and phosphodiesterase activities. When cells once depleted on ATP by treatment with 2,4-dinitrophenol (1 mM; 10 min) were washed and suspended in fresh buffer, the ATP level was recovered almost fully in 10 min. This recovery coincided with the restoration of responsiveness to insulin. When cells were incubated with [125I]iodoinsulin or insulin for 5 min at 15 degrees instead of 37 degrees, a negligible quantity of radioactivity accumulated in Peak 2 and insulin failed to activate sugar transport. In contrast, under the same conditions, radioactivity accumulated in Peak 1 and insulin stimulated phosphodiesterase considerably. These results suggest that ATP, or some other compound metabolically related to ATP, may be necessary for the actions of insulin on sugar transport and phosphodiesterase. ATP, or some other related compound, may also be necessary in the formation of the radioactive Peak 2, although the physiological function and cellular location of this peak are yet to be ascertained.