Salmon calcitonin (sCT) suppresses small intestinal transit (SIT) or motility, but
the mechanism is not well understood. Bolus s.c. administration of a pharmacologic
dose of sCT (140 IU/kg) to mice significantly decreased plasma calcium and phosphorus,
and suppressed SIT from 1 to 8 h for plasma calcium and phosphorus or 20 h for SIT
(respective maximal effects were seen at 5 h, between 2 and 8 h, and between 1 and
5 h). Significant SIT inhibition did not occur at doses smaller than 140 IU/kg. Reverse
transcription-polymerase chain reactions and Southern analysis demonstrated high levels
of calcitonin receptor mRNA in diencephalon and lung, moderate levels of mRNA in cerebellum,
kidney, and muscle, and barely detectable amounts in cerebral cortex and thymus. No
message was detectable in duodenum, jejunum, liver, testis, or heart. Specific binding
of [125I] sCT was demonstrated in the diencephalon. Intracerebroventricular (i.c.v.) administration
of sCT inhibited SIT time- and dose-dependently. Maximal inhibition was obtained at
a dose of 4 IU/kg, 20 mm after injection. Pretreatment with sCT (140 IU/kg s.c.) completely
abolished inhibition of SIT by i.c.v. sCT (4 IU/kg). These results suggest that sCT
binds to receptors in the central nervous system and inhibits small bowel transit.
Key words
Salmon Calcitonin - Small Intestinal Transit - Calcitonin Receptor - Intracerebroventricular
Administration - Central Nervous System
