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The density of beta-endorphin receptors and the proportions of fibres that expressed the receptors was assessed in fast extensor digitorum longus muscle and slow soleus muscles of normal and dystrophic mice using [125I]beta-endorphin and autoradiography. In the EDL the density was approximately 3.5 times higher and the proportion of labelled fibres approximately 2.6 times higher in dystrophic mice than normal mice. In the soleus the density was approximately 6.4 times higher and the proportion of labelled fibres approximately 1.5 times higher in the dystrophic mice than the normal mice. The receptors were of the delta-opioid subtype.

Specific binding sites for [125I]beta-endorphin and the delta1-opioid [3H][D-pen(2), D-pen(5)]enkephalin (DPDPE) were quantified using autoradiography in soleus and extensor digitorum longus (EDL) muscles of lean and obese-diabetic (ob/ob) mice. The density of binding was significantly higher in obese-diabetic than lean mice. The uptake of 2-deoxy-D-[1-3H]deoxyglucose, a nonmetabolized glucose analogue, into isolated soleus and EDL muscles was stimulated by beta-endorphin, beta-endorphin 1-27, and DPDPE, but not by the delta2-opioid deltorphin II. Both beta-endorphin and DPDPE stimulated deoxyglucose uptake in obese-diabetic mice. Thus, glucose transport in skeletal muscle may be partly mediated via delta1-opioid receptors. The increased receptor density in obese-diabetic mice may be an adaptive response., (Copyright 2001 by W.B. Saunders Company)

The uptake of 2-[3H]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.

Autoradiography was used to demonstrate beta-endorphin and delta-opioid receptors in muscles of normal and obese-diabetic mice. The density of the receptors was significantly higher in the obese-diabetic mice. In both normal and diabetic mice, glycolytic and oxidative fibers exhibited the beta-endorphin receptors. However, a significantly greater density of beta-endorphin receptors was observed in the extensor digitorum longus muscles than in the soleus muscles in the diabetic mice. In normal muscles the beta-endorphin receptors were largely restricted to regions where endplates were present, but in the obese-diabetic mice they were densely distributed along the length of the muscle fibers.

Autoradiography was used to study the opioid receptors in soleus and extensor digitorum longus (EDL) muscles from normal mice and mice with type II diabetes. Binding sites for [125I]beta-endorphin were present on the surface membranes in muscles from normal mice. The density of receptors was higher in muscles from obese diabetic mice. The specific delta-opioid ligands DPDPE and [D-Ala2]deltorphin-II inhibited the binding of [125I]beta-endorphin whereas mu and kappa agonists did not. Therefore, the opioid receptor present in skeletal muscle fibers of the mouse is of the delta subtype and the number of these receptors is increased in type II diabetes in the mouse.