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GiprKO mice fed moderate high-fat diet did not display weight gain. On the other hand, GiprKO mice fed high carbohydrate (ST) showed weight gain and did not display obvious glucose intolerance. Glucose-induced insulin secretion was enhanced during intraperitoneal glucose tolerance tests and from isolated islets in both WT and GiprKO mice fed ST compared with those fed normal chow.
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Glp1r/gipr double knockout mice have higher insulin clearance than WT mice, following intravenous injection of glucose. This suggests that incretin hormones reduce insulin clearance at physiological, nonstimulated levels.
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The study provides evidence that the insulinotropic action of zfGIP in mammalian systems involves activation of both the GLP-1 and the GIP receptors but not the glucagon receptor
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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.
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Microarray analysis revealed that pregnancy-specific glycoprotein 17 (Psg17), a potential CD9-binding partner, was significantly decreased in GIP receptor-knockout (Gipr-/-) testes.
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GIPR signaling in adipose tissue plays a critical role in high fat diet-induced insulin resistance and hepatic steatosis in vivo, which may involve IL-6 signaling.
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Genetic deletion of both GLP-1 and GIP receptors reveals that they are required to maintain an adequate islet number in adulthood and to maintain normal beta cell responses to glucose.
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Results suggest the beneficial effects of glucose-dependent insulinotropic polypeptide on periodontal disease.
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Gipr(-/-) offspring of mice exposed to high fat diet(HFD) during pregnancy/lactation became insulin resistant and obese and exhibited increased adipose tissue inflammation and decreased peripheral tissue substrate utilization after reintroduction of HFD.
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Beta-cell Gipr KO mice exhibit lower levels of meal-stimulated insulin secretion, decreased expansion of adipose tissue mass and preservation of insulin sensitivity and decreased TCF1 expression.
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Gipr is expressed in healthy arteries, predominantly in endothelial cells.
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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
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Functional GIP receptors play a major role in islet compensatory response to high fat feeding in mice.
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our data demonstrate that the expression of GLP-1R and GIPR is regulated by glucose concentrations in MC3T3-E1 cells undergoing differentiation induced by BMP-2.
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Results show that GIPR undergoes trafficking between the plasma membrane and intracellular compartments of both GIP-stimulated and unstimulated adipocytes.
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Structural and pharmacological characterization of novel potent and selective monoclonal antibody antagonists of glucose-dependent insulinotropic polypeptide receptor.
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a role of the adipocyte GIPr in nutrient-dependent regulation of body weight and lean mass, but it does not support a direct and independent role for the adipocyte or beta-cell GIPr in promoting adipogenesis.
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Gipr is essential for adrenal steroidogenesis and links high fat (HF) feeding to increased levels of corticosterone, reduced glucocorticoid levels do not significantly contribute to the enhanced metabolic phenotypes in HF-fed Gipr(-/-) mice.
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GIPR(dn) transgenic mice show a disturbed expansion of the endocrine pancreas, due to perturbed islet neogenesis.
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GIP receptors play an important role in cognition, neurotransmission, and cell proliferation.
