Abstract
We investigated the mechanism by which 3,5-diiodo-l-thyronine (T2) affects skeletal muscle mitochondrial bioenergetic parameters following its acute administration to hypothyroid rats. One hour after injection, T2 increased both coupled and uncoupled respiration rates by +27% and +42%, respectively. Top-down elasticity analysis revealed that these effects were the result of increases in the substrate oxidation and mitochondrial uncoupling. Discriminating between proton-leak and redox-slip processes, we identified an increased mitochondrial proton conductance as the "pathway" underlying the effect of T2 on mitochondrial uncoupling. As a whole, these results may provide a mechanism by which T2 rapidly affects energy metabolism in hypothyroid rats.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
-
Cell Respiration / drug effects
-
Diiodothyronines / administration & dosage*
-
Diiodothyronines / pharmacology*
-
Energy Metabolism / drug effects*
-
Hypothyroidism / metabolism*
-
Kinetics
-
Male
-
Malonates / pharmacology
-
Membrane Potential, Mitochondrial / drug effects
-
Mitochondria, Muscle / drug effects*
-
Mitochondria, Muscle / metabolism*
-
Muscle, Skeletal / drug effects
-
Muscle, Skeletal / metabolism*
-
Oligomycins / pharmacology
-
Oxidation-Reduction / drug effects
-
Phosphorylation / drug effects
-
Protons
-
Rats
-
Rats, Wistar
Substances
-
Diiodothyronines
-
Malonates
-
Oligomycins
-
Protons
-
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
-
3',5'-diiodothyronine
-
malonic acid