Abstract
Mammalian skeletal muscles are composed of two major fibre types (I and II) that differ in terms of size, metabolism and contractile properties. In general, slow-twitch type I fibres are rich in mitochondria and have a greater insulin sensitivity than fast-twitch type II skeletal muscles. Although not widely appreciated, a forced induction of the slow skeletal muscle phenotype may inhibit the progress of obesity and diabetes. This potentially forms the basis for targeting slow/oxidative myofibers in the treatment of obesity. In this context, a better understanding of the molecular basis of fibre-type specification and plasticity may help to identify potential therapeutic targets for obesity and diabetes.
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