The effect of calcitonin on food intake in diabetic mice

The characteristic hyperphagia of the genetically obese diabetic (C57Bl/Ks-db+/db+) mouse (db/db) is thought to be due to defect in the satiety circuitry with a secondary overproduction of a circulating satiety factor to which they are insensitive. Recent studies have suggested that calcitonin may be a potent hormonal mediator of the satiety reflex. In this study it was shown that db/db mice were eight fold more sensitive to calcitonin than their heterozygote littermate controls. Mice with streptozotocin-induced diabetes were ten-fold more sensitive to calcitonin than their littermate controls. These results show that diabetes increases the sensitivity to the satiety effects of calcitonin.