Evidence for a hormonal action of beta-endorphin to increase glucose uptake in resting and contracting skeletal muscle

The uptake of 2-[H-3]deoxyglucose, a non-metabolisable derivative of glucose, was studied in resting and contracting muscle. An isolated phrenic nerve/hemidiaphragm preparation of the mouse was used, and contractions of the muscle were elicited by electrical stimulation of the nerve. beta-Endorphin stimulated the uptake of 2-deoxyglucose in resting diaphragm muscle. The rate of uptake in the presence of the optimum concentration of beta-endorphin was similar to that in the presence of the optimum concentration of insulin over the short incubation period. beta-Endorphin also stimulated the uptake of 2-deoxyglucose in contracting muscle, but the optimum concentration of the peptide for this effect was three orders of magnitude lower than in resting muscle. The optimum concentration for insulin, however, was similar in resting and contracting muscle. An analogue of the C-terminal tetrapeptide of beta-endorphin also stimulated 2-deoxyglucose uptake, but this peptide was equally efficacious in resting and contracting muscle. It is suggested that beta-endorphin, which is released into the circulation during exercise, may have a hormonal action to increase the uptake of glucose during muscular activity. This peptide or its metabolites may be partly responsible for the insulin-independent uptake of glucose during exercise.