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Gastric inhibitory polypeptide

This gene encodes an incretin hormone and belongs to the glucagon superfamily. The encoded protein is important in maintaining glucose homeostasis as it is a potent stimulator of insulin secretion from pancreatic beta-cells following food ingestion and nutrient absorption. This gene stimulates insulin secretion via its G protein-coupled receptor activation of adenylyl cyclase and other signal transduction pathways. It is a relatively poor inhibitor of gastric acid secretion. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Glucagon, Insulin, E4, DSP, HAD
Papers using GIP antibodies
Gastric inhibitory polypeptide modulates adiposity and fat oxidation under diminished insulin action.
Kocher Olivier, In PLoS ONE, 2004
... mice were then infused with human GIP(1–42) (25 nmol/kg/day, Abgent, San Diego, CA) or ...
Papers on GIP
Glucagon-like peptide-1 and gastric inhibitory polypeptide: new advances.
Gallwitz, Tübingen, Germany. In Curr Opin Endocrinol Diabetes Obes, Feb 2016
PURPOSE OF REVIEW: Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) are gastrointestinal peptides that play an important role as incretin hormones in the regulation of plasma glucose and insulin secretion.
Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery.
Madsbad et al., Copenhagen, Denmark. In Am J Physiol Endocrinol Metab, Feb 2016
UNASSIGNED: Exaggerated secretion of glucagon-like peptide 1 (GLP-1) is important for postprandial glucose tolerance after Roux-en-Y gastric bypass (RYGB), whereas the role of glucose-dependent insulinotropic polypeptide (GIP) remains to be resolved.
A Protein Preload Enhances the Glucose-Lowering Efficacy of Vildagliptin in Type 2 Diabetes.
Rayner et al., Adelaide, Australia. In Diabetes Care, Feb 2016
OBJECTIVE: Nutrient "preloads" given before meals can attenuate postprandial glycemic excursions, at least partly by slowing gastric emptying and stimulating secretion of the incretins (i.e., glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]).
Cardiovascular Effects of Incretin-Based Therapies.
Baker et al., Farmington, United States. In Annu Rev Med, Feb 2016
These agents prolong the action of the incretin hormones, GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), by inhibiting their breakdown.
TCF1 links GIPR signaling to the control of beta cell function and survival.
Drucker et al., Toronto, Canada. In Nat Med, Jan 2016
The glucagon-like peptide-1 (GLP-1) receptor and the glucose-dependent insulinotropic polypeptide (GIP) receptor transduce nutrient-stimulated signals to control beta cell function.
Incretin actions and consequences of incretin-based therapies: lessons from complementary animal models.
Wolf et al., München, Germany. In J Pathol, Jan 2016
The two incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP1), were discovered 45 and 30 years ago.
Pancreatic glucose-dependent insulinotropic polypeptide (GIP) (1-30) expression is upregulated in diabetes and PEGylated GIP(1-30) can suppress the progression of low-dose-STZ-induced hyperglycaemia in mice.
Haneda et al., Asahikawa, Japan. In Diabetologia, Jan 2016
AIMS/HYPOTHESIS: Glucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone released from gut K cells.
The effect of pregnane X receptor agonists on postprandial incretin hormone secretion in rats and humans.
Savolainen et al., Oulu, Finland. In J Physiol Pharmacol, Dec 2015
We now aimed to determine if the secretion of incretin hormones, especially glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), are affected by PXR agonists since these gut-secreted hormones are major regulators of postprandial glucose metabolism.
New perspectives on exploitation of incretin peptides for the treatment of diabetes and related disorders.
Flatt et al., Coleraine, United Kingdom. In World J Diabetes, Dec 2015
This review highlights the therapeutic potential of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), oxyntomodulin (OXM) and cholecystokinin (CCK) for obesity-related diabetes.
Incretin therapies - highlighting common features and differences in the modes of action of GLP-1 receptor agonists and DPP-4 inhibitors.
Nauck, Bochum, Germany. In Diabetes Obes Metab, Nov 2015
In patients with T2D, pharmacological doses/concentrations of GLP-1 can compensate for the inability of diabetic beta-cells to respond to the main incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), and thus is a suitable parent compound for incretin-based glucose-lowering medications.
A rationally designed monomeric peptide triagonist corrects obesity and diabetes in rodents.
Tschöp et al., München, Germany. In Nat Med, 2015
We report the discovery of a new monomeric peptide that reduces body weight and diabetic complications in rodent models of obesity by acting as an agonist at three key metabolically-related peptide hormone receptors: glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon receptors.
Guanine nucleotide binding protein-like 3 is a potential prognosis indicator of gastric cancer.
Zhang et al., Taizhou, China. In Int J Clin Exp Pathol, 2014
Guanine nucleotide binding protein-like 3 (GNL3) is a GIP-binding nuclear protein that has been reported to be involved in various biological processes, including cell proliferation, cellular senescence and tumorigenesis.
Pharmacology, physiology, and mechanisms of incretin hormone action.
Drucker et al., Toronto, Canada. In Cell Metab, 2013
Incretin peptides, principally GLP-1 and GIP, regulate islet hormone secretion, glucose concentrations, lipid metabolism, gut motility, appetite and body weight, and immune function, providing a scientific basis for utilizing incretin-based therapies in the treatment of type 2 diabetes.
A VGF-derived peptide attenuates development of type 2 diabetes via enhancement of islet β-cell survival and function.
Newgard et al., Durham, United States. In Cell Metab, 2012
TLQP-21 prevents islet cell apoptosis by a pathway similar to that used by GLP-1, but independent of the GLP-1, GIP, or VIP receptors.
Guanine nucleotide-binding protein Gαi2: a new partner of claudin-5 that regulates tight junction integrity in human brain endothelial cells.
Couraud et al., Paris, France. In J Cereb Blood Flow Metab, 2012
Galphai2 as a novel claudin-5 partner required for TJ integrity in brain endothelial cells.
Fasting and oral glucose-stimulated levels of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are highly familial traits.
Hansen et al., Copenhagen, Denmark. In Diabetologia, 2012
The results suggest that circulating levels of GIP and GLP-1 as well as the beta cell response to these incretins are highly familial as compared with fasting and stimulated plasma glucose, serum insulin and serum C-peptide levels.
Elevated plasma glucose-dependent insulinotropic polypeptide associates with hyperinsulinemia in metabolic syndrome.
Rabuazzo et al., Catania, Italy. In Eur J Endocrinol, 2012
Hyperinsulinemia subjects with metabolic syndrome showed increased GIP secretion that could be responsible for the delayed glucagon suppression.
Impaired incretin-induced amplification of insulin secretion after glucose homeostatic dysregulation in healthy subjects.
Knop et al., Glostrup, Denmark. In J Clin Endocrinol Metab, 2012
Data suggest that reduced insulinotropic effect of GIP or GLP-1 (as in type 2 diabetes) can be induced in healthy subjects; this indicates that reduced incretin stimulation of insulin secretion results from insulin resistance/glucose intolerance.
Different incretin responses after pancreatoduodenectomy and distal pancreatectomy.
Tanaka et al., Fukuoka, Japan. In Pancreas, 2012
The changes in glucose metabolism and incretin (GLP-1/GIP) responses were different between pancreatoduodenectomy and distal pancreatectomy.
GPCR interacting proteins (GIPs) in the nervous system: Roles in physiology and pathologies.
Fagni et al., Montpellier, France. In Annu Rev Pharmacol Toxicol, 2009
Recently, roles of GPCR-GIP interactions in central nervous system physiology and pathologies have been revealed.
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