Long-term and short-term changes in mitochondrial parameters by thyroid hormones.

Abstract

In the hyperthyroid state, delta psi m, delta pHm and therefore delta p are increased in rat liver. An enhanced delta p accords with a higher energy output. The subcellular distribution of adenine nucleotides in different thyroid states does not reflect the driving force for mitochondrial adenine-nucleotide translocase (that is delta psi m). Therefore, a change in delta psi m cannot be solely responsible for the postulated stimulation of adenine-nucleotide transport by THs. This is also the case for the changes in delta pHm, and in the subcellular distribution of malate, 2-oxoglutarate and glutamate, that are observed under the influence of THs. T3 induces calcium influx into the liver cell within minutes. It increases respiration and gluconeogenesis with the same kinetics. Therefore, it is suggested that, as with glucagon and vasopressin, calcium is the mediator of these changes. The delta p is increased with T3 and glucagon treatment but not with vasopressin. The changes in delta psi m and delta pHm appear to be the result of the individual actions of these hormones on ATP-consuming and ATP-producing reactions. The delta psi p is only increased with T3 treatment. This is related to the different mechanisms of enhancing intracellular calcium that are used by vasopressin, glucagon and T3.