gastric inhibitory polypeptide

The last receptor binds gastric inhibitory polypeptide.

Gastric inhibitory polypeptide receptors are seven-transmembrane proteins found on beta-cells in the pancreas.

Staurosporine stimulated the response to both histamine and gastric inhibitory polypeptide in the absence of TPA.

Gastric inhibitory polypeptide (GIP)

In the absence of TPA, staurosporine enhanced the response to gastric inhibitory polypeptide by 49 (14) % (Table I).

Gastric inhibitory polypeptide (GIP), also known as the glucose-dependent insulinotropic peptide is a member of the secretin family of hormones.

New information is also provided on the modulation of the activity of the gastric inhibitory polypeptide and TGLP-1 receptors in HGT-1 cells.

HGT-1 cells also express receptors for vasoactive intestinal polypeptide, gastric inhibitory polypeptide and for TGLP-1.

The actions of the gastric inhibitory polypeptide receptor on adenylate cyclase seems to be under the control of an activated form of Gi in HGT-1 cells.

GLP1R binds specifically the glucagon-like peptide-1 (GLP1) and has much lower affinity for related peptides such as the gastric inhibitory polypeptide and glucagon.

During a meal the incretins glucagon-like peptide 1 (GLP-1) and glucose-dependent gastric inhibitory polypeptide (GIP) are released from the small intestine into the vasculature.

Gastric inhibitory polypeptide (GIP), also called glucose-dependent insulinotropic polypeptide, is a 42-amino acid polypeptide synthesized by K cells of the duodenum and small intestine.

The cyclic AMP response to 100 nmol/l gastric inhibitory polypeptide was enhanced by preincubation with TPA, while the responses to cholera toxin and forskolin were unaffected.

The gastric inhibitory polypeptide receptor (GIP-R) also known as the glucose-dependent insulinotropic polypeptide receptor is a protein that in humans is encoded by the GIPR gene.

Additionally, the effect of fibre on other gastrointestinal hormones such as gastric inhibitory polypeptide, vasoactive intestinal polypeptide and glucagon may be important, probably through their effect on insulin and its antinatriuretic role (Anderson, 1980).

Furthermore, the inhibitor of protein kinase C, staurosporine, completely prevented the effects of TPA on stimulation of the cyclic AMP content by histamine, TGLP-1, and gastric inhibitory polypeptide.

It is well known that glucose lowering effects of DPP-4 inhibitors are mainly mediated by GLP-1 and gastric inhibitory polypeptide (GIP) incretin hormones which are inactivated by DPP-4.

At maximally effective concentrations of peptides (100 nmol/l), preincubation with 100 nmol/l TPA reduced the cyclic AMP response to TGLP-1 and enhanced the response to gastric inhibitory polypeptide.

To enable the identification of the sites of action of protein kinase C, the actions of TPA on the cyclic AMP response to histamine, gastric inhibitory polypeptide, TGLP-1, cholera toxin, and forskolin have been compared.

Preincubation of layers of attached HGT-1 cells in culture flasks in the presence of 500 ng/ml of pertussis toxin for two hours before detachment prevented the effects of TPA on the resposne to gastric inhibitory polypeptide.

Octreotide is an analog of the peptide hormone somatostatin, which inhibits the production of the growth hormone as well as numerous peptide hormones of the gastrointestinal system, including insulin, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide, and gastrin.

Preincubation with pertussis toxin prevented the enhancement of the gastric inhibitory polypeptide response by TPA, suggesting an involvement of an inhibitory guanine nucleotide regulatory subunit of the Gi class, but did not change the inhibition of histamine stimulation.

The prevention by pertussis toxin of the stimulatory effect of TPA on the action of gastric inhibitory polypeptide suggests an involvement of a guanine nucleotide binding protein of the class designated Gi in this action of TPA.

Preincubation with staurosporine abolished the stimulatory effect of 100 nmol/l TPA on the response to 100 nmol/l gastric inhibitory polypeptide and the inhibitory effect of TPA on the response to TGLP-1 (Table I).

The HGT-1 gastric cancer cell line was used to determine the actions of protein kinase C on the stimulation of adenylate cyclase by the human histamine H 2 receptor, and the receptors for gastric inhibitory polypeptide and truncated glucagon like peptide 1 (TGLP-1).