Glucagon immunoreactivity in plasma from normal and dystrophic mice.

Abstract

The present investigation was undertaken to determine and characterize glucagon immunoreactivity in plasma from normal NMRI mice and from dystrophic mice and their unaffected littermates of the 129/ReJ strain. Very young dystrophic mice (6 weeks old) displayed much higher basal levels of plasma glucagon immunoreactivity than normal mice. In contrast, plasma concentrations of insulin and glucose were lower in these dystrophic mice than in normal NMRI mice. The plasma glucagon levels declined with age in both strains during the time-period studied (1.5–5 months). Gel filtration of plasma from dystrophic as well as normal mice on Sephadex G-200 revealed that a large part of the total glucagon immunoreactivity was eluted in fractions containing the immunoglobulins. The amount of the ‘true’ glucagon part was lower in plasma from normal mice (about 0.2 μg/l) than in plasma from mice of the dystrophic strain (0.4–0.5 μg/l)). This finding was indirectly corroborated by the observation that a large intravenous glucose load decreased plasma glucagon by approximately 0.2 μg/l in the non-dystrophic NMRI strain and by about 0.4–0.6 μg/l in the dystrophic strain. Thus, the ability of glucose to suppress glucagon secretion appeared unaffected in the dystrophic mice. Glucose-induced insulin release, however, was considerably impaired in these animals. It is concluded that mice of the dystrophic 129/ReJ strain have higher plasma levels of ‘true’ glucagon than mice of the non-dystrophic NMRI strain. Whether the abnormally high plasma glucagon levels in the dystrophic strain, particularly in very young dystrophic mice, might contribute to the development of the muscular dystrophy remains to be elucidated.