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The genetic variability of GIP gene is associated with coronary artery disease and it may play a role in the premature coronary artery disease in the Chinese Han population with type 2 diabetes.
Describe model, in which the release of GIP/GLP-1 (show GCG Proteins) is stimulated by glucose in the proximal small intestine, and no differences in the secretion dynamics between healthy individuals and patients with T2D are identified after taking differences in glucose profiles into account.
The ability of a truncated form of GIP, GIP(3-30)NH2, to antagonize the physiological actions of GIP in glucose metabolism, subcutaneous abdominal adipose tissue blood flow, and lipid metabolism in humans.
Compared with the lean group, the obese group had significantly higher fasting and post-OGTT GIP levels, but similar fasting GLP-1 (show GCG Proteins) and significantly lower post-OGTT GLP-1 (show GCG Proteins) levels.
GIP and PP plasma concentrations are lower in pancreatic cancer irrespective of the degree of glucose intolerance as compared to Type 2 diabetic patients and healthy controls.
Evening postprandial insulin (show INS Proteins) and GIP responses and insulin (show INS Proteins) resistance declined by over 30% after three meals that limited daily carbohydrate intake to 30% compared to no such changes after three 60%-carbohydrate meals, an effect that was independent of pre-meal exercise.
the stimulatory effect of IGF-1 (show IGF1 Proteins) on GIP promoter support the hypothesis of a functional growth hormone (show GH1 Proteins)-igf-1 (show IGF1 Proteins)-GIP axis
decreased maternal 25OHD may be associated with decreased cord 25OHD and increased cord GLP-1 (show GCG Proteins) and GIP levels, which may be involved with the transfer of maternal glucose to the fetus
Excess androgen activity might be a factor contributing to alter secretion of incretins in lean polycystic ovary syndrome (PCOS) women. However it could not be ruled out that it is also possible that increased GIP levels might induce hyperandrogenemia in PCOS.
Our results might indicate an altered DPP4 (show DPP4 Proteins)-incretin system and altered immunoregulation including a potentially dysfunctional GLP1 (show GCG Proteins)(9)(-)(36) signaling in T1DM.
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.
GIP provides a novel link between the immune system and the gut (show GUSB Proteins), with proinflammatory-immune modulatory function but minor glucose regulatory relevance in the context of acute endotoxemia.
our data suggest that the metabolic hormone GIP plays an important role in bone marrow hematopoiesis
these findings identify distinct roles for DPP4 (show DPP4 Proteins) in the endothelial cell versus the bone marrow compartment for selective incretin degradation and DPP4 (show DPP4 Proteins) inhibition-mediated glucoregulation.
These results strongly suggest that incretins upregulate the TNF-alpha-stimulated IL6 synthesis in osteoblasts, and that the amplifying effect of incretin is exerted via reducing the IkappaB/NFkappaB pathway through the adenylyl cyclase-cAMP system.
It was demonstrated that cardiomyocytes represent a direct target of GIP action in vitro, and that GIP ameliorated AngII-induced cardiac hypertrophy via suppression of cardiomyocyte enlargement, apoptosis, and fibrosis in vivo.
Galanin (show GAL Proteins), acting via the GAL1 (show LGALS1 Proteins) receptor and Gi -coupled signalling in L and K cells, is a potent inhibitor of GLP-1 (show GCG Proteins) and GIP secretion
The loss of food-induced GIP response in Roux-limb of intestine likely contributes to the attenuated serum GIP response to feeding.
GIP induces the expression of the proatherogenic cytokine osteopontin (OPN (show SPP1 Proteins)) in mouse arteries via local release of endothelin-1 (show EDN1 Proteins) and activation of CREB (show CREB1 Proteins). GIPR (show GIPR Proteins) mRNA is higher in symptomatic carotid endarterectomy patients.
These studies support the hypothesis that a reduction in GIP signaling using a GIP-neutralizing mAb might provide a useful method for the treatment and prevention of obesity and related disorders.
RYGB in lean pigs increases the response of GIP, total GLP-1 (show GCG Proteins), and insulin (show INS Proteins), but reduces levels of active GLP-1 (show GCG Proteins) in response to an oral glucose load. These data challenge the role of active GLP-1 (show GCG Proteins) as a contributor to remission from diabetes after RYGB
porcine GIP stimulated the proliferation of MC-26 cells, a mouse CRC (show RYR1 Proteins) cell line, in a concentration-dependent manner.
The patterns of colocalisation of the K cell marker, glucagon-like insulinotropic peptide, and the L cell markers, glucagon like peptide-1 and peptide YY, in enteroendocrine cells of the small intestine and colon of mouse and pig, were investigated.
Preferentially catalyzes the dephosphorylation of 'Ser- 5' within the tandem 7 residues repeats in the C-terminal domain (CTD) of the largest RNA polymerase II subunit POLR2A. Negatively regulates RNA polymerase II transcription, possibly by controlling the transition from initiation/capping to processive transcript elongation (By similarity). Recruited by REST to neuronal genes that contain RE-1 elements, leading to neuronal gene silencing in non-neuronal cells.
glucose-dependent insulinotropic polypeptide
, gastric inhibitory polypeptide
, incretin hormone
, Glucose-dependent insulinotropic peptide