The
hormones amylin and
calcitonin interact with receptors within the same family to exert their effects on the human organism.
Calcitonin, derived from thyroid C cells, is known for its inhibitory effect on osteoclasts.
Calcitonin of mammalian origin promotes
insulin sensitivity, while the more potent
calcitonin extracted from salmon additionally inhibits gastric emptying, promotes gallbladder relaxation, increases energy expenditure and induces satiety as well as
weight loss.
Amylin, derived from pancreatic beta cells, regulates plasma
glucose by delaying gastric emptying after meal ingestion, and modulates
glucagon secretion and central satiety signals in the brain. Thus, both
hormones seem to have metabolic effects of relevance in the context of
non-alcoholic fatty liver disease (
NAFLD) and other
metabolic diseases. In rats, studies with dual
amylin and
calcitonin receptor agonists have demonstrated robust
body weight loss, improved
glucose tolerance and a decreased deposition of fat in liver tissue beyond what is observed after a
body weight loss. The translational aspects of these preclinical data currently remain unknown. Here, we describe the physiology, pathophysiology, and pharmacological effects of
amylin and
calcitonin and review preclinical and clinical findings alluding to the future potential of
amylin and
calcitonin-based drugs for the treatment of
obesity and
NAFLD.