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Data suggest that GIPR (gastric inhibitory polypeptide receptor) is among the few GPCRs (G-protein-coupled receptors) which signal through G-proteins (GTP-binding protein Gs alpha subunit (show GNAS Proteins), here) both at plasma membrane and in endosomes; recombinant proteins expressed in HEK293 cells were used in these studies.
GIPR overexpression does not appear to affect acromegalic patients' clinical features
Study shows the internalization of GIPR involving clathrin-coated pits, AP-2 (show GTF3A Proteins) and dynamin (show DNM1 Proteins) and its subsequent intracellular trafficking. GIP (show GIP Proteins) stimulates a rapid robust internalization of the GIPR, the major part being directed to lysosomes.
The common variant rs10423928 in the GIPR gene is associated with increased risk of stroke in patients with type 2 diabetes.
Body mass index change for the A/T+A/A in GIPR genotypes was significantly higher than that for the T/T genotype. rs10423928 may predict weight gain in schizophrenia.
The potential future role of gastric inhibitory peptide (GIP (show GIP Proteins)) receptors as molecular targets in neuroendocrine neoplasms may be dependent on the tumor grade.
Results show that GIPR undergoes trafficking between the plasma membrane and intracellular compartments of both GIP (show GIP Proteins)-stimulated and unstimulated adipocytes.
GIPR is overexpressed in gastric and duodenal neuroendocrine tumors
GIPR expression was downregulated in subcutaneous adipose tissue from obese patients and correlated negatively with body mass index, waist circumference, systolic blood pressure, and glucose and triglyceride levels.
GIPR promoter was hypomethylated in type 2 diabetic patients as compared to controls.
GIP stimulation induces a switch in GIPR recycling from a rapid endosomal to a slow trans-Golgi network (TGN) pathway. GPCR kinases and b-arrestin2 are required for this switch in recycling.
Microarray analysis revealed that pregnancy-specific glycoprotein 17 (Psg17), a potential CD9 (show CD9 Proteins)-binding partner, was significantly decreased in GIP (show GIP Proteins) receptor-knockout (Gipr-/-) testes.
GIPR signaling in adipose tissue plays a critical role in high fat diet-induced insulin (show INS Proteins) resistance and hepatic steatosis in vivo, which may involve IL-6 (show IL6 Proteins) signaling.
Genetic deletion of both GLP-1 (show GCG Proteins) and GIP (show GIP Proteins) receptors reveals that they are required to maintain an adequate islet number in adulthood and to maintain normal beta cell responses to glucose.
Results suggest the beneficial effects of glucose-dependent insulinotropic polypeptide (show GIP Proteins) on periodontal disease.
Gipr(-/-) offspring of mice exposed to high fat diet(HFD) during pregnancy/lactation became insulin (show INS Proteins) resistant and obese and exhibited increased adipose tissue inflammation and decreased peripheral tissue substrate utilization after reintroduction of HFD.
Beta-cell Gipr KO mice exhibit lower levels of meal-stimulated insulin (show INS Proteins) secretion, decreased expansion of adipose tissue mass and preservation of insulin (show INS Proteins) sensitivity and decreased TCF1 (show HNF1A Proteins) expression.
Gipr is expressed in healthy arteries, predominantly in endothelial cells.
These data highlighted the importance of intact GIPR signalling and dietary composition in modulating memory and learning, and hippocampal pathways involved in the maintenance of synaptic plasticity
Functional GIP (show GIP Proteins) receptors play a major role in islet compensatory response to high fat feeding in mice.
Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin (show INS Proteins) by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide (show GIP Proteins))/GIP (show GIP Proteins) receptor signaling.
This gene encodes a G-protein coupled receptor for gastric inhibitory polypeptide (GIP), which was originally identified as an activity in gut extracts that inhibited gastric acid secretion and gastrin release, but subsequently was demonstrated to stimulate insulin release in the presence of elevated glucose. Mice lacking this gene exhibit higher blood glucose levels with impaired initial insulin response after oral glucose load. Defect in this gene thus may contribute to the pathogenesis of diabetes.
gastric inhibitory polypeptide receptor
, glucagon receptor
, gastric inhibitory polypeptide receptor-like
, glucose-dependent insulinotropic polypeptide receptor
, gastric inhibitory peptide receptor