Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stimulus-secretion coupling of the insulin-producing pancreatic islet beta cell is subject to functional maturation during fetal life. We studied the maturation of a glucose-responsive insulin release from fetal rat islets and specifically investigated the impact of peptidergic regulation. To this end, islets were isolated from 21-day-old fetal rats and maintained for 7 days in tissue culture at 3.3 or 11.1 mM glucose and various supplements. In islets cultured in low glucose, acutely raising the ambient glucose concentration to 16.7 mM evoked a modest stimulation of short-term insulin release that was more pronounced in islets maintained in high glucose. Moreover, the insulin content was much higher in islets cultured in high than in low glucose. Culture with growth hormone (GH) markedly amplified both basal and stimulated short-term insulin secretion from islets maintained in either low or high glucose. Additionally, GH significantly elevated the insulin content in islets maintained in low glucose. Transforming growth factor alpha (TGF-alpha) increased basal, but not glucose-stimulated, insulin release and insulin content in islets cultured in low glucose. Gastrin, expressed in islets during fetal life, did not affect basal or glucose-stimulated insulin release, or insulin content, in islets maintained in either low or high glucose. The addition of gastrin to TGF-alpha did not affect the results obtained with the latter peptide. Gastrin-releasing peptide failed to influence basal or glucose-responsive insulin secretory rates, and insulin content, at either glucose concentration during culture. The somatostatin analog Sandostatin (octreotide acetate) neither influenced basal nor stimulated short-term insulin release at any glucose concentration present during culture, whereas the hormone significantly decreased the insulin content of islets cultured in high glucose. Pancreastatin, produced by porcine islet beta and delta cells, failed to influence basal or glucose-responsive insulin secretory rates, and islet insulin content, at either glucose concentration during culture. Culture with gastric inhibitory peptide (GIP) or glucagon-like peptide I (GLP-1), two proposed incretins, did not affect short-term insulin secretion in response to 3.3 or 16.7 mM glucose irrespective of the ambient glucose concentration during culture. To the contrary, GLP-1, but not GIP, increased the content of insulin in islets cultured in low glucose. We conclude that islet beta-cell differentiation and functional maturation of the stimulus-secretion coupling can be modulated in vitro in fetal rat pancreatic tissue by peptidergic regulation and glycemic stimulation. We suggest that GH and TGF-alpha stimulate, while somatostatin, through paracrine interaction, may inhibit, these processes. These effectors may be of regulatory significance in the in vivo development of glucose-sensitive beta cells, and defects in these mechanisms may result in glucose intolerance in adult subjects.
Pancreas 2000 Apr
PMID:Peptidergic regulation of maturation of the stimulus-secretion coupling in fetal islet beta cells. 1076 55

A 71-year-old man with duodenal gastrin cell tumor was being evaluated for residual/metastatic disease. Somatostatin receptor scintigraphy (SRS) identified a 2-cm area of focal uptake within the head of the pancreas, consistent with a pancreatic neuroendocrine tumor. Pathological examination did not reveal any malignancy within the pancreas. Instead, the pancreatic head showed pancreatic polypeptide cell hyperplasia. Strong and diffuse immunoreactivity to somatostatin receptor 2A antibody by immunoperoxidase staining confirmed that the lesion correlated with the site of radioactive tracer (Indium-111 pentetreotide) uptake seen on SRS. The current report therefore presents pancreatic polypeptide cell hyperplasia as a new pitfall in SRS.
Pancreas 2007 Nov
PMID:Indium-111 pentetreotide uptake by pancreatic polypeptide cell hyperplasia: potential pitfall in somatostatin receptor scintigraphy. 1809 Feb 46

Carcinoid Tumours are classified as Neuro-endocrine tumours. Commonly known ulcerogenic neuro-endocrine tumour is Gastrinoma of the Pancreas and Duodenum.It secretes hormone Gastrin which causes hyperplasia of the gastric parietal cells with excessive secretion of hydrochloric acid resulting in multiple ulcerations in the stomach, duodenum and upper jejunum. Carcinoid tumours is not known to cause peptic ulceration.
 ...
PMID:Recurrent Peptic Ulcer due to Carcinoid Tumour of Jejunum. 2285 46

A 74-year-old man with recurrent duodenal ulcers underwent somatostatin receptor scintigraphy (SRS) in suspicion of gastrinoma. A 2-cm area of focal uptake was visualized within the pancreatic head. Serum chromogranin A levels were elevated, but serum gastrin levels and the secretin test were normal. Computed tomography and endoscopic ultrasonography were not conclusive. After partial duodenopancreatectomy, pathological examination failed to reveal any neuroendocrine tumor. Instead, the dorsal portion of the pancreatic head was found to be densely populated by pancreatic polypeptide cell-rich islets. This area correlated with the site of tracer uptake seen on SRS. Thus, pancreatic polypeptide cell-rich islets in elderly patients should be kept in mind when interpreting SRS results to avoid unnecessary major pancreatic resections.
Pancreas 2014 May
PMID:Pancreatic polypeptide-rich islets in the posterior portion of the pancreatic head--a tumor mimic in somatostatin receptor scintigraphy. 2471 72

Our group observed the first case of synchronous gastric neuroendocrine tumor (NET) and duodenal gastrinoma with autoimmune chronic atrophic gastritis (CAG), in the absence of Helicobacter pylori infection. Demographic, clinical, endoscopic, and pathologic data were abstracted from the electronic medical record at Mount Sinai Hospital from 2013 to 2015. The patient's anonymity was carefully protected, and informed consent was obtained for publication of protected health information. A 53-year-old woman with hypertension presented to Mount Sinai Hospital in June 2013 for a second opinion for management of gastric and duodenal NETs. After evaluation by gastroenterology and surgery, repeat upper endoscopy with ultrasound and fine-needle aspiration revealed multiple diminutive type I gastric NETs and 2 duodenal NETs, against a background of autoimmune CAG, with biopsy pathology negative for H. pylori. She subsequently underwent a transduodenal resection of the duodenal NETs, confirming low-grade, gastrin-positive, stage T2 duodenal NET. On routine follow-up over the next 2 years, clinical, radiographic, and endoscopic surveillance revealed no recurrent or metastatic gastric or duodenal disease. This first report of synchronous duodenal gastrinoma and gastric NET in the setting of autoimmune CAG can broaden our understanding of gastric NET pathophysiology.
Pancreas 2019 01
PMID:Gastric Neuroendocrine Tumor and Duodenal Gastrinoma With Chronic Autoimmune Atrophic Gastritis. 3053 Dec 43


<< Previous 1 2 3 4 5