GLP-1 and GIP are hormones that increase insulin production and decrease glucagon production when nutrients are consumed, which helps control blood glucose levels.

In mice with obesity and diabetes, a modified version of the hormone GLP-1 called (Abu8)GLP-1 lowers blood sugar and increases insulin production more than two other related hormones, suggesting this chemical change improves its ability to act against diabetes in living organisms.

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.

Modified versions of GLP-1 and GIP hormones that resist breakdown by DPP IV lower blood glucose more effectively in diabetic mice than the natural versions, and the location of a specific amino acid change (Abu8 in GLP-1) results in the strongest effect.

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.