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Am J Physiol Renal Physiol 280: F95-F102, 2001;
0363-6127/01 $5.00
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Vol. 280, Issue 1, F95-F102, January 2001

Short-term K+ deprivation provokes insulin resistance of cellular K+ uptake revealed with the K+ clamp

Cheol S. Choi, Curtis B. Thompson, Patrick K. K. Leong, Alicia A. McDonough, and Jang H. Youn

Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California 90089-9142

We aimed to test the feasibility of quantifying insulin action on cellular K+ uptake in vivo in the conscious rat by measuring the exogenous K+ infusion rate needed to maintain constant plasma K+ concentration ([K+]) during insulin infusion. In this "K+ clamp" the K+ infusion rate required to clamp plasma [K+] is a measure of insulin action to increase net plasma K+ disappearance. K+ infusion rate required to clamp plasma [K+] was insulin dose dependent. Renal K+ excretion was not significantly affected by insulin at a physiological concentration (~90 µU/ml, P > 0.05), indicating that most of insulin-mediated plasma K+ disappearance was due to K+ uptake by extrarenal tissues. In rats deprived of K+ for 2 days, plasma [K+] fell from 4.2 to 3.8 mM, insulin-mediated plasma glucose clearance was normal, but insulin-mediated plasma K+ disappearance decreased to 20% of control, even though there was no change in muscle Na-K-ATPase activity or expression, which is believed to be the main K+ uptake route. After 10 days K+ deprivation, plasma [K+] fell to 2.9 mM, insulin-mediated K+ disappearance decreased to 6% of control (glucose clearance normal), and there were 50% decreases in Na-K-ATPase activity and alpha 2-subunit levels. In conclusion, the present study proves the feasibility of the K+ clamp technique and demonstrates that short-term K+ deprivation leads to a near complete insulin resistance of cellular K+ uptake that precedes changes in muscle sodium pump expression.

skeletal muscle; Na-K-ATPase isoforms; hypokalemia


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