Interesting abstract: Thyroid hormone effects on mitochondrial energetics

[Guest guest]

Thyroid. 2008 Feb;18(2):145-56.

PMID: 18279015 [PubMed - in process]

Thyroid hormone effects on mitochondrial energetics.

Harper ME, Seifert EL.

Department of Biochemistry, Microbiology, and Immunology, Faculty of

Medicine, University of Ottawa, Ottawa, Ontario, Canada.

Thyroid hormones are the major endocrine regulators of metabolic

rate, and

their hypermetabolic effects are widely recognized. The cellular

mechanisms

underlying these metabolic effects have been the subject of much

research.

Thyroid hormone status has a profound impact on mitochondria, the

organelles

responsible for the majority of cellular adenosine triphosphate (ATP)

production. However, mechanisms are not well understood. We review the

effects of thyroid hormones on mitochondrial energetics and principally

oxidative phosphorylation. Genomic and nongenomic mechanisms have been

studied. Through the former, thyroid hormones stimulate

mitochondriogenesis

and thereby augment cellular oxidative capacity. Thyroid hormones induce

substantial modifications in mitochondrial inner membrane protein and

lipid

compositions. Results are consistent with the idea that thyroid hormones

activate the uncoupling of oxidative phosphorylation through various

mechanisms involving inner membrane proteins and lipids. Increased

uncoupling appears to be responsible for some of the hypermetabolic

effects

of thyroid hormones. ATP synthesis and turnover reactions are also

affected.

There appear to be complex relationships between mitochondrial proton

leak

mechanisms, reactive oxygen species production, and thyroid status.

As the

majority of studies have focused on the effects of thyroid status on rat

liver preparations, there is still a need to address fundamental

questions

regarding thyroid hormone effects in other tissues and species.