1980 Volume 23 Issue 3 Pages 227-233
To determine whether or not the pancreatic A cell dysfunction observed in diabetics is reversible, plasma glucagon responses to an oral glucose load, arginine infusion and insulin-induced hypoglycemia were investigated before and after diabetic treatment in 15 adult onset diabetic patients consisting of 10 men and 5 women. Along with the plasma glucagon (GI), the responses of plasma C-peptide (CPR) and blood glucose were also studied under the same circumstances.
The fasting blood glucose concentration was decreased from 219±14 mg/dl (the value before treatment) to 120±5 mg/dl after treatment, and the peak value of the blood glucose during OGTT prior to treatment, 400±18 mg/dl, fell significantly after treatment reaching a corresponding value of 282±14 mg/dl. A significant difference was observed in the plasma CPR concentrations at 90 min (p<0.05) and 120 min (p<0.01) during OGTT before and after treatment.ΣCPR, the incremental area of the plasma CPR, was significantly increased from 130±34 ng·min/dl. (the value before treatment) to 276±56 ng·min/dl after treatment (p<0.05). The plasma GI level was not suppressed during OGTT either before or after treatment in the diabetics. Thus, the pancreatic B cell response to hyperglycemia was significantly improved, but the A cell function to the same stimulus revealed no remarkable change after treatment. The exaggerated response of plaima glucagon to i.v. arginine was reduced following appropriate treatment.ΣGI, the incremental area of the plasma GI, was decreased from 9901±1567 pg·min/ml (the value before treatment) to 7366±1224 pg·min/m/ after treatment, but the difference between these values was not statistically significant. After treatment, the plasma CPR response to i.v. arginine was increased and consequently a significant augmentation of ΣCPR resulted.
The patients revealed a minimal level of blood glucose at 45 to 60 min after insulin injection. The blood glucose before and after the treatment during ITT showed nadirs of 46±4 mg/dl and 36±4 mg/dl, respectively. The latter value was significantly lower than the former (p<0.05), though both fall into the hypoglycemic range. The rate of blood glucose fall was similar in both situations. No significant change in plasma GI level was observed during ITT before the treatment, but it was significantly elevated after the treatment from an initial level of 130±11 pg/ml to a peak of 176±14 pg/m/ at 90 min. Also, the plasma GI values at 45, 60, 90 and 120 min were significantly higher than the initial level in the controlled patients. Likewise, ΣGI was significantly increased after the treatment, showing values of 1158±556 pg·min/ml before treatment and 3318±795 pg·min/ml after treatment (p<0.05). These results indicate that not only the B cell but also the A cell dysfunctions encountered in uncontrolled diabetics are reversible in part after treatment.
