Skeletal muscle glucose metabolism appears to be regulated by locally
derived factors as well as by systemically circulating hormones. Local
factors may be particularly important during exercise, when substrate
demand can increase rapidly. Numerous studies in perfused limbs sugge
st that the kallikrein-kinin system may participate in the regulation
of substrate delivery and utilization by skeletal muscle. Evidence als
o suggests that kinins mediate the increase in insulin sensitivity aft
er administration of converting enzyme inhibitors. Tissue kallikrein h
as been isolated and purified from rat skeletal muscles, and its level
is highest in muscle with high oxidative activity. In other tissues,
kallikrein synthesis is under the influence of insulin. It has not bee
n possible to demonstrate effects of kallikrein or kinins on glucose m
etabolism in isolated skeletal muscle or cardiocytes. Therefore modula
tion of glucose metabolism by kallikrein or kinins may only be observe
d in intact perfused tissues or organs.