Erschienen in:
01.04.2007 | Commentary
Mitochondrial function: use it or lose it
verfasst von:
J. A. Hawley, S. J. Lessard
Erschienen in:
Diabetologia
|
Ausgabe 4/2007
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Excerpt
Type 2 diabetes is a progressive metabolic disorder that develops as a result of both environmental and undefined genetic factors [
1]. While the precise molecular aetiology of this disorder remains elusive, there is general consensus that type 2 diabetes has several hallmark features: (1) a breakdown in lipid and carbohydrate metabolism, reflected by elevated levels of circulating metabolites and culminating in excessive deposition of fat in various tissues [
2]; (2) skeletal muscle insulin resistance [
3]; and (3) coordinated defects in oxidative metabolism [
4‐
6]. In conjunction with these altered metabolic states is the impaired insulin signalling observed in muscle of patients with type 2 diabetes [
7]. At present, it is unclear whether these (and other) defects are a consequence of the diabetic state or are instrumental in its development. Unravelling this puzzle is made more difficult because these impairments do not occur in isolation but typically co-exist in the same individual. …