Gastric Inhibitory Polypeptide
Mostrando 1-12 de 22 artigos, teses e dissertações.
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1. ARMC5 mutations are associated with high levels of proliferating cell nuclear antigen and the presence of the serotonin receptor 5HT4R in PMAH nodules
ABSTRACT Objective To analyze the morphological and functional characteristics of primary macronodular adrenal hyperplasia (PMAH) nodules carrying or not carrying ARMC5 mutations and the consequences of the presence of mutations in terms of the pattern of macronodule composition and functional state. Subjects and methods The analyses were performed by he
Arch. Endocrinol. Metab.. Publicado em: 2020-08
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2. Estudo da expressão dos receptores do peptídeo insulinotrópico dependente de glicose (GIPR) e do hormônio luteinizante (LHCGR) em tumores e hiperplasias do córtex adrenal / Expression Study of Glucose-dependent insulinotropic peptide receptor (GIPR) and luteinizing hormone receptor (LHCGR) in adrenocortical tumors and hyperplasia
Introduction: The glucose- dependent insulinotropic peptide receptor (GIPR) and luteinizing hormone receptor (LHCGR) are G-protein coupled receptors with a wide tissue expression pattern. The aberrant expression of these receptors has been described in cases of ACTH-independent macronodular adrenal hyperplasia (AIMAH) and in some adenomas, resulting in the i
Publicado em: 2007
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3. The diversity of abnormal hormone receptors in adrenal Cushing's syndrome allows novel pharmacological therapies
Recent studies from several groups have indicated that abnormal or ectopic expression and function of adrenal receptors for various hormones may regulate cortisol production in ACTH-independent hypercortisolism. Gastric inhibitory polypeptide (GIP)-dependent Cushing's syndrome has been described in patients with either unilateral adenoma or bilateral macrono
Brazilian Journal of Medical and Biological Research. Publicado em: 2000-10
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4. The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.
The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a concentration of 25 ng/ml produced a prompt, but transi
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5. Vasoactive intestinal polypeptide: a putative transmitter in the canine gastric muscularis mucosa.
The nature of the inhibitory transmitter in the canine gastric muscularis mucosae was studied in vitro using superfusion techniques. The inhibitory effect of nerve stimulation (10 V, 200 mus, 10 Hz) was not altered by adrenergic, cholinergic or serotonergic antagonists. Adenosine triphosphate had no effect on spontaneous mechanical activity. Nucleotide pyrop
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6. Interaction of Fat-stimulated Gastric Inhibitory Polypeptide on Pancreatic Alpha and Beta Cell Function
Gastric inhibitory polypeptide (GIP) is considered to be the principal mediator of the enteroinsular axis. A glucose-insulin clamp technique was used to study the effects of differing blood glucose levels on the insulinotropic and glucagonotropic actions of fat-stimulated GIP in seven healthy subjects, as well as the effect of physiologic hyperinsulinemia on
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7. Sequence of an intestinal cDNA encoding human gastric inhibitory polypeptide precursor.
Gastric inhibitory polypeptide (GIP) is a 42-amino acid hormone that stimulates insulin secretion in the presence of glucose. Complementary DNA clones encoding human GIP were isolated from a library prepared with RNA from duodenum. The predicted amino acid sequence indicates that GIP is derived by proteolytic processing of a 153-residue precursor, preproGIP.
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8. Effect of gastric inhibitory polypeptide on plasma levels of chylomicron triglycerides in dogs.
To determine whether gastric inhibitory polypeptide (GIP) promotes the clearance of chylomicron triglycerides (TG) from the circulation in dogs, chyle collected from donor dogs via a thoracic duct fistula was infused at a rate of 2 ml/min i.v. into normal recipient dogs during an infusion of either porcine GIP (1 microgram/kg per h) or saline as a control. I
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9. Glucose intolerance caused by a defect in the entero-insular axis: A study in gastric inhibitory polypeptide receptor knockout mice
Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic β cells. GIPR−/− mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. Although blood glucose levels after meal inge
The National Academy of Sciences.
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10. Oral Glucose Augmentation of Insulin Secretion: INTERACTIONS OF GASTRIC INHIBITORY POLYPEPTIDE WITH AMBIENT GLUCOSE AND INSULIN LEVELS
Gastric inhibitory polypeptide, or GIP, has been postulated as the major enteric hormonal mediator of insulin release. The release of immuno-reactive GIP (IR-GIP) after oral glucose and its role in insulin release was studied in normal men by the glucose clamp technique. In 24 subjects studied with the hyperglycemic clamp, blood glucose was maintained at 125
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11. Effects of the vagus nerves on gastric motility and release of vasoactive intestinal polypeptide in the anaesthetized lamb.
1. Effects of the vagus nerves on the activity of the reticulo-omasal orifice (ROO) and the abomasum and the concentration of vasoactive intestinal polypeptide (VIP) in gastric and intestinal venous effluent were studied in anaesthetized lambs. 2. Both excitatory and inhibitory effects of the vagus on the ROO and abomasum were demonstrated. Excitation of act
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12. Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs.
Previous studies comparing the effects of oral, intraportal, and peripheral venous administration of glucose in conscious dogs demonstrated a significant increase in hepatic extraction of insulin only after oral glucose, but similar hepatic uptake of glucose after oral and intraportal glucose, which was greater than that after peripheral intravenous glucose