| First Author | Yamada Y | Year | 2006 |
| Journal | Diabetes | Volume | 55 Suppl 2 |
| Pages | S86-91 | Mgi Jnum | J:120775 |
| Mgi Id | MGI:3707950 | Doi | 10.2337/db06-S011 |
| Citation | Yamada Y, et al. (2006) Pancreatic and extrapancreatic effects of gastric inhibitory polypeptide. Diabetes 55 Suppl 2:S86-91 |
| abstractText | The hormonal factor(s) implicated as transmitters of signals from the gut to pancreatic beta-cells is referred to as incretin, and gastric inhibitory polypeptide (GIP) is identified as one of the incretins. GIP is a gastrointestinal peptide hormone of 42 amino acids that is released from duodenal endocrine K-cells after absorption of glucose or fat and exerts its effects by binding to its specific receptor, the GIP receptor. By generating and characterizing mice with a targeted mutation of the GIP receptor gene, we have shown that GIP has not only an insulinotropic role, but also physiological roles on fat accumulation into adipose tissues and calcium accumulation into bone. We here propose a new acronym, GIP, for gut-derived nutrient-intake polypeptide. |
