Pancreatic Islet
The insulin and glucagon-producing cells. Incretin drugs raise insulin here only when glucose is already high, which is why they do not cause hypoglycaemia on their own the way injected insulin does.
Relationships
2 connectionsPancreatic Islet expressed in
GIP Receptor
The second incretin receptor. Adding it to GLP-1 agonism is what separates tirzepatide from semaglutide: more energy expenditure and a direct effect on fat tissue, on top of the appetite drop.
GLP-1 Receptor
The incretin receptor behind semaglutide and every drug in that class. Three separate effects run through it: appetite suppression in the brain, slower stomach emptying, and glucose-dependent insulin release from the pancreas.
Beyond this page
Pancreatic Islet also connects to 3 entries in the applied modules, covering supplements, compounds, hormones and food sources. Those carry the mechanism and the evidence tier behind each link, and they are part of client coaching.
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