Mauritio
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- Feb 26, 2018
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It has long been shown that T3 increases uncoupling ,but this study shows that it also works vice versa :
Uncoupling (through BAT activation) increases deiodinase type 2 ,which catalyzes T4 toT3 conversion .
This should create a positive feedback loop. If you uncouple your metabolism with aspirin for example ...
Salicylic Acid Is an Uncoupler and Inhibitor of Mitochondrial Electron Transport
...this will increase deiodinase type 2 ,which will increase T3 ,which will increase UCP1 ,which will increase uncoupling,...
"Vice versa, sympathetic stimulation of BAT triggers the expression of deiodinase type II, an enzyme that enhances local thyroid hormone availability and signaling"
Thyroid hormones in the regulation of brown adipose tissue thermogenesis - PubMed
This might be important as T3 has other ways of increasing glucose consumption and thermogenesis that are not related to uncoupling:
"Consequently, the metabolic and thermogenic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents."
(Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption - PubMed)
Interestingly T3 and UCP1 don't raise free radicals . Which has to with their increase in autophagy . They both help to get rid of old mitochondria and create new ones .
This study shows that blocking autophagy leads to an increase in free radicals and a decrease in metabolism by T3 .
"T3 increased fatty acid oxidation and mitochondrial respiration as well as autophagic flux, mitophagy, and mitochondrial biogenesis. Interestingly, there was no significant induction of intracellular reactive oxygen species (ROS) despite high mitochondrial respiration and UCP1 induction by T3. However, when cells were treated with Atg5 siRNA to block autophagy, induction of mitochondrial respiration by T3 decreased, and was accompanied by ROS accumulation, demonstrating a critical role for autophagic mitochondrial turnover."
(Thyroid hormone (T 3) stimulates brown adipose tissue activation via mitochondrial biogenesis and MTOR-mediated mitophagy - PubMed)
Uncoupling (through BAT activation) increases deiodinase type 2 ,which catalyzes T4 toT3 conversion .
This should create a positive feedback loop. If you uncouple your metabolism with aspirin for example ...
Salicylic Acid Is an Uncoupler and Inhibitor of Mitochondrial Electron Transport
...this will increase deiodinase type 2 ,which will increase T3 ,which will increase UCP1 ,which will increase uncoupling,...
"Vice versa, sympathetic stimulation of BAT triggers the expression of deiodinase type II, an enzyme that enhances local thyroid hormone availability and signaling"
Thyroid hormones in the regulation of brown adipose tissue thermogenesis - PubMed
This might be important as T3 has other ways of increasing glucose consumption and thermogenesis that are not related to uncoupling:
"Consequently, the metabolic and thermogenic effects of systemic hyperthyroidism were maintained in UCP1 knockout mice, demonstrating that neither beige nor brown fat contributes to the TH-induced hyperthermia and elevated glucose consumption, and underlining that the mere presence of UCP1 is insufficient to draw conclusions on the therapeutic potential of browning agents."
(Thyroid-Hormone-Induced Browning of White Adipose Tissue Does Not Contribute to Thermogenesis and Glucose Consumption - PubMed)
Interestingly T3 and UCP1 don't raise free radicals . Which has to with their increase in autophagy . They both help to get rid of old mitochondria and create new ones .
This study shows that blocking autophagy leads to an increase in free radicals and a decrease in metabolism by T3 .
"T3 increased fatty acid oxidation and mitochondrial respiration as well as autophagic flux, mitophagy, and mitochondrial biogenesis. Interestingly, there was no significant induction of intracellular reactive oxygen species (ROS) despite high mitochondrial respiration and UCP1 induction by T3. However, when cells were treated with Atg5 siRNA to block autophagy, induction of mitochondrial respiration by T3 decreased, and was accompanied by ROS accumulation, demonstrating a critical role for autophagic mitochondrial turnover."
(Thyroid hormone (T 3) stimulates brown adipose tissue activation via mitochondrial biogenesis and MTOR-mediated mitophagy - PubMed)
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