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It is important to note that in human subjects these are merely observational and coincident changes in multiple signaling pathways; causal relationships between impairments in oxidative metabolism and mitochondrial function with insulin resistance is not established (), and indeed there is evidence that in the condition of primary congenital insulin resistance, mitochondrial dysfunction follows ().

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Ablation of GLUT4 specifically in skeletal muscle led to glucose intolerance and severe impairments in insulin-mediated glucose disposal into muscle in mice as young as 8 weeks of age ().

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Though aon the UKPDS showed that just being in the intervention group reduced heart attacks and strokes 10 years after the follow up period, imagine how many heart attacks and strokes might have been prevented had patients maintained glycemic control over a much longer period of time!

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In the skeletal muscle, insulin increases glucose transport, permitting glucose entry and glycogen synthesis.

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Retroviral delivery of short hairpin RNA into 3T3L1 adipocytes yielding reduced Lcn2 expression was associated with improved insulin action while exogenous Lcn2 promoted insulin resistance in cultured hepatocytes ().

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