Plasma glucagon and glucagon-like immunoreactive components in Type 1 (insulin-dependent) diabetic patients and normal subjects before and after an oral glucose load.

Biogel P-30 filtration of plasma from Type 1 (insulin-dependent) diabetic patients and normal subjects in basal state and after an oral glucose load was assayed with a C-terminal (30 K) and a glucagon-like immunoreactivity-cross-reacting antiserum (R8). Up to four immunoreactive peaks of approximate molecular sizes of greater than 20,000 (fraction I), 9000 (fraction II), 3500 (fraction III) and 2000 (fraction IV) were detected with the two antisera in both groups. In the basal state, the only significant difference observed between both groups was a higher R8-reactivity in fraction II in the group of diabetic patients, although the R8 minus 30 K values for this fraction did not show a significant difference between both groups. After glucose the only significant differences were an increase of R8-reactivity in fraction II in both groups (p less than 0.01) and a decrease of 30 K-reactivity in fraction III (IRG3500) in normal subjects (p less than 0.05). In seven out of 12 diabetic patients, 30 K-reactivity in fraction II (IRG9000) and III (IRG3500) increased above their basal values. The gut-glucagon-like immunoreactivity response to oral glucose (delta R8-delta 30 K values in fraction II) was similar in both the diabetic and normal subjects. These results indicate that the paradoxical rise in plasma immunoreactive glucagon after oral glucose in diabetic patients may be due to an increase of both IRG3500 and/or IRG9000, the gut-glucagon-like immunoreactivity released during glucose absorption has a molecular weight of approximately 9000, and no differences in plasma gut-glucagon-like immunoreactivity were observed in Type 1 diabetic patients when compared with normal subjects, either in the basal state or after glucose ingestion.