Evidence against a specific effect of serum from patients with cystic fibrosis on sodium-dependent glucose transport in the rat jejunum.

Sera from patients with cystic fibrosis of the pancreas (CF) and normal 
human sera were assayed for the ability to inhibit sodium- dependent 
glucose transport in rat brush-border membrane vesicles. Fresh CF and age- 
and sex-matched control sera were both inhibitory when compared to physiologic 
saline. The inhibition by CF serum was 44 +/- 13% (mean 
+/- SD) at a final serum concentration of 6.7%, 67 +/- 
34% at 10% serum, and 68 +/- 28% at 20% serum. 
The ratio of the inhibition of CF sera compared to that 
of control sera was 1.00, 0.78, and 0.93 at 6.7, 10, 
and 20% serum concentrations, respectively. Although a slightly greater inhibition by 
CF serum was observed at a concentration of 10%, this is 
probably not significant because no difference could be detected at a 
concentration of 20% serum. Glucose transport in the presence of serum 
was sensitive to phlorizin indicating that the residual glucose transport was 
proceeding by the sodium-dependent glucose transport system. These findings suggest that 
CF serum does not specifically inhibit the sodium-dependent glucose transport system. 
The intravesicular space accessible to glucose was reduced in the presence 
of CF or control serum. Fresh CF serum was 1.4 times 
more effective than fresh control serum (P less than 0.01). The 
presence of substantial vesicle- shrinking activity in control serum indicates that 
this activity cannot be considered specific for CF. 