Inhibition of Insulin Action on Glucose Uptake into Skeletal Muscle by a Kallikrein-Trypsin Inhibitor

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Abstract
The effect of insulin on glucose metabolism of skeletal muscle was studied in the human forearm by the determination of the arterial concentrations of oxygen, glucose, free fatty acids, .beta.-hydroxybutyrate, acetoacetate, the deep-venous concentrations of oxygen, glucose, insulin and the forearm blood flow in 11 healthy volunteers during a basal period and a 30 min infusion of insulin into the brachial artery (250 .mu. units .times. kg-1 .times. min-1). Arterial concentration of glucose was maintained by i.v. infusion of glucose (1 mg .times. kg-1 .times. min-1). During the infusion of insulin 5 of the subjects received a (i.v.) kallikrein-trypsin inhibitor (875,000 KIU[kallikrien inhibitor unit]/45 min). Under the influence of the inhibitor the insulin-induced acceleration of glucose uptake was about halved throughout the whole test period (P < 0.05 - P < 0.005). Suitably comparable clinical data, almost identical substrate supply and identical deep-venous insulin concentration in both groups proved the observed effect to be real and not due to methodological causes. Since there is no evidence so far that proteases are involved in insulin action, inhibitor-induced reduction of kinin liberation from kininogen was suggested to be responsible for the reduced effect of insulin. The kallikrein-kinin system may be involved in the translation of insulin action on glucose metabolism in skeletal muscle.

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