Infusion of insulin directly into thyroid arterial blood perfusing the surgically
isolated in situ pig thyroid gland produced an increase in the secretion rate of calcitonin (CT) measured
by immunoassay in thyroid venous effluent blood. Insulin in concentrations ranging
from approximately 1 to 400 ng/ml produced a maximal stimulation of 4 - 5 fold. The
stimulatory effect of insulin on CT could not be duplicated by infusion of either
IGF-I or amylin. Specific binding of radiolabeled insulin was demonstrated using isolated
pig thyroid plasma membranes and both rat (6-23) and human (TT) medullary thyroid
carcinoma C-cells. Increased CT release was observed from C-cells exposed to a high
concentration of insulin. The administration of glucose iv to pigs in order to stimulate
secretion of endogenous insulin produced an increase in circulating insulin, which
was accompanied by an increase in the secretion of CT. The results show that insulin,
delivered directly to the pig thyroid gland, can stimulate CT release. The in vitro binding and secretion studies indicate that C-cells can bind insulin and respond
with an increase in CT secretion, and the iv glucose experiments suggest that endogenous
insulin is capable of stimulating CT secretion. The findings imply that insulin is
capable of acting as a CT secretagogue and suggest that changes in CT secretion may
accompany altered states of insulin production such as diabetes or insulin-secreting
tumors.
Key words
Insulin - Calcitonin - Diabetes - Calcium - Bone
