Endocrine Abstracts

We have previously shown that β-endorphin reduces muscle fatigue and increases glucose uptake in contracting and non-contracting skeletal muscles of the mouse. The aim of this study was to compare the effect of these peptides on glucose uptake and muscle fatigue in normal mice and obese-diabetic mice (which provide a model for non insulin-dependent diabetes mellitus, NIDDM). The uptake of glucose into contracting and non-contracting muscle was assessed using the non-metabolised glucose analogue [3H]2-deoxy-glucose. Muscle contractions were elicited by high frequency (tetanic) electrical stimulation of the phrenic nerve, in isolated phrenic nerve-hemidiaphragm preparations and muscle tension was measured using a force transducer.

β-Endorphin stimulated the uptake of DOG in non-contracting muscles of normal mice but not obese-diabetic mice, but it stimulated glucose uptake in contracting muscles from both normal and diabetic mice.

Intravenous β-Endorphin caused a significant reduction in blood glucose in obese-diabetic mice.

In normal mice, the fatigue developed in response to high frequency stimulation of the phrenic nerve was significantly lower in the presence of β-endorphin in males but not in females. Insulin had no significant effect on fatigue in mice of either sex. β-Endorphin reduced fatigue in muscles of the diabetic mice.

β-Endorphin is released from the pituitary into the blood during exercise and this peptide could be responsible for the (insulin-independent) uptake of glucose which occurs in exercising muscle. The peptide could have therapeutic use in diabetes to improve glucose homeostasis and reduce muscle fatigue.