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The molecular events leading to activation or silencing of glucose-sensitive neurons are surprisingly similar to those of the endocrine pancreas and include neuronal uptake of glucose via GLUT2, conversion to pyruvate (and finally ATP) via glucokinase, and modulation of neuronal firing mediated by changes in K ATP channel activity, cell depolarisation and Ca 2+ influx

This rapid skeletal muscle tissue damage and intramuscular infiltration of immune cells contribute to PEM-related symptoms

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