Adiponectin is not required for exercise training‐induced improvements in glucose and insulin tolerance in mice

Abstract Adiponectin (Ad) is a potent insulin‐sensitizing adipokine that has been found to activate pathways involved in the adaptation to exercise. Therefore, we examined whether Ad is required for the increased insulin response observed following exercise training in Ad knockout mice (Ad KO ). Eight weeks of exercise training significantly increased glucose and insulin tolerance in both wild type ( WT ) and Ad KO mice. There were no differences in glucose tolerance between genotypes but insulin tolerance was improved to a greater extent in Ad KO compared to WT mice following exercise training (+26%, P  < 0.05). There were no genotype differences in the insulin‐stimulated phosphorylation of AKT or AS 160 in red or white gastrocnemius muscle ( RG , WG ). Exercise training increased total AKT and AS 160 protein content in RG and total AS 160 protein content in WG . There were no genotype differences in total AKT or AS 160. However, exercise training induced a more robust increase in total AS 160 in RG from Ad KO (+44 ± 8%, P  < 0.05) compared to WT mice (+28 ± 7%, P  = 0.06). There were no differences in total GLUT 4 or FAT / CD 36 in RG or WG in WT or Ad KO , with or without exercise training. Similarly, there were no differences in RER , VO 2 , or activity between any groups. Our results indicate the presence of Ad is not required for exercise‐induced increases in insulin response. Furthermore, it appears that exercise may improve insulin sensitivity to a greater extent in the absence of Ad, suggesting the presence of an unknown compensatory mechanism.