Background: Somatostatin-14 is present in breast milk, and intact somatosta
tin-14 has been recovered from gastric lumen of infants. Studies have shown
that somatostatin-14 is metabolized in the intestinal luminal contents in
vitro, which could be prevented by the presence of breast milk. In this stu
dy, the effect of milk on stability of somatostatin-14 in suckling rat jeju
num in vivo was examined.
Methods: I-125-Somatostatin-14[Tyr 11] was administered to the isolated jej
unal loops in anesthetized suckling rats in the absence or presence of milk
, fractions of milk, or known protease-peptidase inhibitors. Structural int
egrity of I-125-somatostatin-14[Tyr 11] recovered from tissues at different
intervals was analyzed by gel filtration and high-performance liquid chrom
atography.
Results: Radioactivity rapidly disappeared from the jejunal lumen with a 50
% clearance achieved by 1.2 minutes. Gel filtration and high-performance li
quid chromatography analyses showed that I-125-somatostatin-14[Tyr 11] was
rapidly degraded into smaller fragments. At 1 minute, jejunal luminal radio
activity was eluted in a major peak with retention time of 42.4 minutes, al
ong with other minor peaks (retention time, 5.6, 8.0, 10.4, and 14.4 minute
s); only a trace amount of intact I-125- somatostatin-14[Tyr 11] (retention
time, 44.8 minutes) was present. Coadministration of rat's milk or its sol
uble fraction increased the level of intact I-125-somatostatin-14[Tyr 11] i
n the jejunal lumen and jejunal tissue. Presence of rat's milk-casein or pe
ptidase inhibitors (bestatin, phosphoramidon, or Bowman-Birk inhibitor), ho
wever, failed to increase the level of intact I-125-somatostatin-14[Tyr 11]
.
Conclusion: These results suggest that somatostatin-14 is rapidly degraded
in the jejunal lumen of suckling rats, and that milk-borne peptidase inhibi
tors prevent this somatostatin-14 degradation.