Postexercise skeletal muscle glucose transport is normal in kininogen-deficient rats

Plasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation, or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX, suggesting that normal plasma kininogen is not essential for these important exercise effects.

Male Brown Norway (BN) and Brown Norway Katholiek (BNK; plasma kininogen-deficient) rats were studied. BN and BNK rats were assigned to exercise (4×30-min swim) or sedentary (SED) groups. Rats were anesthetized immediately (0hPEX) or 3 h (3hPEX) after exercise. For 0hPEX and 0hSED rats, one epitrochlearis muscle per rat was used for AMPK phosphorylation and muscle glycogen analyses. The contralateral muscle was incubated with [H]-3-O-methylglucose (3-MG) for GT assay. For 3hPEX and 3hSED rats, one muscle from each rat was incubated without insulin, and the contralateral muscle was incubated with 60 μU·mL insulin, and both muscles were incubated with 3-MG for GT measurement.

This study aimed to determine whether the postexercise (PEX) increase in insulin-dependent or insulin-independent GT is reduced in rats deficient in plasma kininogen versus normal rats.

For 0hPEX versus 0hSED, both BN and BNK rats had greater insulin-independent GT and AMPK phosphorylation with reduced glycogen after exercise. No genotype effects were found 0hPEX. There was a significant main effect of exercise (3hPEX>3hSED) and no interaction between exercise and genotype for basal or insulin-stimulated GT. Conclusions: Plasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation, or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX, suggesting that normal plasma kininogen is not essential for these important exercise effects.