Mitochondrial function in skeletal muscle in type 2 diabetes.

Abstract

Reduced skeletal muscle mitochondrial function has been proposed to lead to insulin resistance and type 2 diabetes. It has been known for several years that oxidative capacity of skeletal muscle is reduced in patients with type 2 diabetes compared to weight matched controls. The reduction in oxidative capacity supposedly leads to the accumulation of intramyocellular lipid which inhibits insulin signalling and causes insulin resistance. It is not known whether this reduction in mitochondrial capacity is the cause or the effect of type 2 diabetes. This PhD-thesis describes the effect of different pharmacological interventions on mitochondrial function in type 2 diabetes and describe whether mitochondrial function is uniformly distributed to both upper and lower extremities. Furthermore, a hypothesis on the molecular mechanism for weight gain observed with anthyperglycaemic treatment will be presented.