In female mice, when the receptors for two specific gut hormones (GIP and GLP-1) are removed, the body no longer releases extra insulin after eating glucose compared to receiving it directly into the...

In female mice, removing the receptors for two gut hormones (GIP and GLP-1) prevents the normal increase in insulin production after eating glucose, reducing the insulin response by about 65% compared to normal mice, showing that these two hormones are responsible for most of the insulin boost triggered by oral glucose in this model.

In female mice, removing the receptors for two gut hormones (GIP and GLP-1) causes blood sugar to rise abnormally after eating sugar, but not after injecting sugar directly into the bloodstream, showing that these hormones are required to regulate blood sugar after meals by helping the liver reduce glucose production.

In female mice, removing receptors for two gut hormones reduces the pancreas's ability to release insulin in response to sugar taken by mouth, but not when sugar is injected directly into the bloodstream, showing that these hormones help the pancreas respond to food entering the gut.

In female mice, removing receptors for GIP and GLP-1 hormones does not stop the pancreas from releasing insulin when glucose is injected into the bloodstream, showing that the pancreas can still detect glucose levels even without these hormonal signals.

People who have multiple autoantibodies targeting their pancreatic islets, but still maintain normal blood sugar levels, show a smaller insulin response to oral glucose compared to intravenous glucose, suggesting an early alteration in how the gut and pancreas communicate.