Abstract
The characteristic hyperphagia of the genetically obese diabetic (C57B1/Ks-db+/db+) mouse (db/db) is thought to be due to a 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.
Original language | English (US) |
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Pages (from-to) | 17-20 |
Number of pages | 4 |
Journal | Peptides |
Volume | 3 |
Issue number | 1 |
DOIs | |
State | Published - 1982 |
Keywords
- Appetite
- Calcitonin
- Diabetes
- db/db Mice