An insulin receptor defect in murine muscular dystrophy.

A study has been made of the I125 insulin binding and postbinding effects on excised soleus muscles from the 129 ReJ strain of dystrophic mice. Results are compared with those in sex- and weight-matched controls. The data suggest that, in the range of physiological hormone concentrations, the affinity of insulin receptors on dystrophic muscles is less than normal and that the insulin-dependent uptake of both 2-deoxyglucose (2-DG) and aminoisobutyric acid (AIB) is impaired. These findings are taken to indicate that many of the biochemical and electrophysiological abnormalities observed in murine dystrophy could arise from some genetic defect in the receptor proteins controlling uptake of raw materials.