[6] GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins,[7] which stimulate insulin release on oral food intake.

However, this is incorrect, as it was discovered that these effects are achieved only with higher-than-normal physiological level, and that these results naturally occur in the body through a similar hormone, secretin.

Researchers at Universities of Angers and Ulster evidenced that genetic ablation of the GIP receptor in mice resulted in profound alterations of bone microarchitecture through modification of the adipokine network.

[14] Furthermore, the deficiency in GIP receptors has also been associated in mice with a dramatic decrease in bone quality and a subsequent increase in fracture risk.

[15] However, the results obtained by these groups are far from conclusive because their animal models give discordant answers and these works should be analysed very carefully.