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Insulin-induced membrane changes in K(+)-depleted rat skeletal muscle
1Department of Physiology, University of Washington, Seattle 98195.
The American Journal of Physiology
|July 1, 1993
Summary
Insulin triggers muscle membrane depolarization in potassium-depleted rats by closing potassium channels and opening sodium channels. This reveals key insights into insulin
Area of Science:
- Muscle physiology
- Cell membrane electrophysiology
- Endocrinology
Background:
- Potassium (K+) depletion significantly alters muscle cell membrane potential.
- Insulin's effects on ion channels in K+-depleted muscle are not fully understood.
Purpose of the Study:
- To investigate insulin-induced membrane potential changes in K+-depleted rat skeletal muscle.
- To elucidate the roles of specific ion channels in these insulin-mediated effects.
Main Methods:
- Inducing K+ depletion in Sprague-Dawley rats via a K+-free diet.
- Measuring muscle membrane potential using electrophysiological techniques.
- Utilizing voltage clamp to analyze K+ currents and ion channel activity, including tetrodotoxin (TTX) sensitivity.
Main Results:
- Combined insulin and low K+ induced significant depolarization in 90% of muscle fibers.
- Tetrodotoxin (TTX) blocked the depolarization, indicating TTX-sensitive Na+ channels.
- Insulin reduced a significant leakage current in K+-depleted fibers, suggesting altered K+ channel function.
Conclusions:
- Insulin-induced depolarization in K+-depleted muscle involves the closure of K+ channels.
- Sustained depolarization is mediated by the opening of non-inactivating, TTX-sensitive Na+ channels.
- These findings highlight altered ion channel behavior in K+-depleted muscle under insulin stimulation.