title: ESCI Award 2006. Mitochondrial function and endocrine diseases.
abstract: Mitochondria are fundamental for oxidative energy production and impairment of their functionality can lead to reduced ATP synthesis and contribute to initiation of apoptosis. Endocrine tissues critically rely on oxidative phosphorylation so that mitochondrial abnormalities may either be causes or consequences of diminished hormone production or action. Abnormalities typical for diseases caused by mitochondrial DNA mutations such as Kearns-Sayre syndrome or mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes syndrome are also seen in certain endocrine diseases. Lack or excess of thyroid hormones, major ubiquitous regulators of mitochondrial content and activity, cause muscular abnormalities and multisystem disorders. Mitochondria are a further prerequisite for steroidogenesis as well as insulin secretion and action. Recent studies showed that reduced mitochondrial ATP synthesis in skeletal muscle is a feature of certain hereditary and acquired forms of insulin resistance and diabetes mellitus. Finally, ageing is not only accompanied by various degrees of hormonal deficiency and insulin resistance but is also associated with a progressive decline of mitochondrial number and function. Future research is needed to examine whether mitochondrial abnormalities are the cause or consequence of ageing and frequent metabolic diseases such as obesity and type 2 diabetes mellitus, and to address mitochondria as a target for novel therapeutic regimes.
authors: Hanusch Hospital, Karl-Landsteiner Institute for Endocrinology and Metabolism, Heinrich Collin Strasse 30, A-1140 Vienna, Austria.
authors: R
authors: R
authors: Stark
authors: M
authors: M
authors: Roden
mesh_terms: D000328:Adult; D017209:Apoptosis; D001692:Biological Transport / Q000502:physiology; D004700:Endocrine System Diseases / Q000378:metabolism*; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D028361:Mitochondrial Diseases / Q000378:metabolism*
chemical_list: D007328:Insulin