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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 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 and significantly lower post-OGTT GLP-1 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 and GIP responses and insulin 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 on GIP promoter support the hypothesis of a functional growth hormone-igf-1-GIP axis
decreased maternal 25OHD may be associated with decreased cord 25OHD and increased cord GLP-1 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-incretin system and altered immunoregulation including a potentially dysfunctional GLP1(9)(-)(36) signaling in T1DM.
Fasting GIP concentrations are higher in individuals with a history of cardiovascular disease (myocardial infarction, stroke) when compared with control subjects.
Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide)/GIP receptor signaling.
Data confirm that postprandial plasma levels of glucose-dependent insulinotropic polypeptide (GIP) and insulin (INS) are responsive to glycemic index of foods consumed; glycemic index of breakfast cereals regulate plasma postprandial GIP and INS.
irisin and GIP might contribute to the development of polycystic ovary syndrome and may also represent novel polycystic ovary syndrome biomarkers
Data suggest that postprandial blood levels of both GIP and insulin can be regulated by diet; here, inclusion of nopal/Opuntia/cactus (a functional food in traditional Mexican medicine) in breakfast reduces postprandial levels of GIP and insulin.
phosphatidylinositol 3-kinase gamma has a role in insulin secretion induced by glucose-dependent insulinotropic polypeptide
These novel results support the notion that the GIP-GIPR axis plays a role in the etiology of central obesity in humans
Data from studies in healthy Japanese men suggest that plasma GIP levels in postprandial period are dose dependently increased by fat content of meals of ordinary size, despite the amount of additional fat being relatively small.
Dietary fructose elicits GLP-1 secretion without simultaneous release of glucagonotropic GIP.
Patients with idiopathic gastroparesis exhibit abnormal GIP levels.
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, 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 in the endothelial cell versus the bone marrow compartment for selective incretin degradation and DPP4 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, acting via the GAL1 receptor and Gi -coupled signalling in L and K cells, is a potent inhibitor of GLP-1 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) in mouse arteries via local release of endothelin-1 and activation of CREB. GIPR 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.
This study provides evidences that GIP acts directly on osteoblasts and is capable of improving collagen maturity and fibril diameter.
There was decrease in GIP gene transcripts and protein in the gut of HNF1a-null mice.
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.
These data indicate that GLP-1 but not GIP is a key mediator of beta cell mass expansion and related adaptations in pregnancy, triggered in part by generation of intra-islet GLP-1.
NUCB2/nesfatin-1 is co-localized with GLP-1 and GIP in small intestinal cells. Data support the hypothesis that nesfatin-1 is present in enteroendocrine cells and that it stimulates incretin secretion.
Circulating levels of GIP were significantly decreased in FABP5-deficient mice.
The results describe key beneficial immunoregulatory properties for glucose-dependent insulinotropic polypeptide in diet-induced obesity and reveal that its augmentation ameliorates adipose tissue inflammation and improves insulin resistance.
GIP-reduced mice demonstrate that partial reduction of GIP does not extensively alter glucose tolerance, but it alleviates obesity and lessens the degree of insulin resistance under high-fat diet conditions, suggesting a potential therapeutic value.
It was concluded from these observations that GIP, but not glucagon-like peptide-1, directly activates PepT1 activity by a cAMP-dependent signaling pathway in jejunum.
RYGB in lean pigs increases the response of GIP, total GLP-1, and insulin, but reduces levels of active GLP-1 in response to an oral glucose load. These data challenge the role of active GLP-1 as a contributor to remission from diabetes after RYGB
porcine GIP stimulated the proliferation of MC-26 cells, a mouse CRC cell line, in a concentration-dependent manner.
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