At first glance, the abovedescribed PPARδ-mediated fuel switching in skeletal muscle would be expectedto give rise to insulin resistance, since a preferential uptake and oxidationof fatty acids (FFAs) over glucose (mediated by PPARδ stimulation in skeletal muscle) would lead to an accumulationof blood glucose, muscle being a major player in blood-glucose homeostasis [1, 2].However, as well as stimulating skeletal muscle fatty acid oxidation, PPARδ plays a surprising role in ameliorating hyperglycemia. This evidence concerns the gene PPARD and Hyperglycemia.