GIP (HUMAN) Chemische Eigenschaften,Einsatz,Produktion Methoden
Beschreibung
GIP was originally isolated as a gastric inhibitory polypeptide. After the discovery of its glucose-dependent insulinotropic activity, known as the incretin effect, GIP was renamed glucose-dependent insulinotropic peptide.
Gastric inhibitory peptide
Abbreviation: GIP
Additional names: gastric inhibitory polypeptide,gastrointestinal inhibitory peptide, glucose-dependent, insulinotropic peptide
Chemische Eigenschaften
Human GIP: Mr 4983.6, theoretical pI 6.92. GIP is soluble in water, but insoluble in ethanol. GIP is inactivated by DPP-4.
History
GIP was originally isolated from the porcine intestinal extract on the basis of its acid inhibitory activity in dogs (gastric inhibitory polypeptide) in the early 1970s, and subsequently renamed glucose-dependent insulinotropic peptide after the finding of its physiologically important role as a potentiator of glucose-stimulated insulin secretion.
Verwenden
GIP possessing incretin activity enhances glucosestimulated insulin release. GIP agonists are potentially useful for the treatment of diabetes. Moreover, DPP-4 inhibitors are approved for use in diabetes patients because GIP is rapidly deactivated by DPP-4.
Biosynthese
The expression of GIP is regulated by nutrients. The administration of glucose and lipid into the rat gastrointestinal tract increases GIP mRNA levels. Circulating GIP levels are low in the fasted state and increase within minutes of food ingestion. The postprandial levels of circulating GIP are dependent on meal size. The degree to which nutrients regulate GIP secretion is speciesdependent. Fat is a more potent stimulator than carbohydrates in humans, whereas in the rodent and pig, carbohydrates are more potent than fat. Once released, GIP is rapidly deactivated by DPP-4.
GIP (HUMAN) Upstream-Materialien And Downstream Produkte
Upstream-Materialien
Downstream Produkte