Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient is described who had a malignant pancreatic islet cell apudoma secreting corticotrophin (ACTH) and melanocyte-stimulating hormone (MSH), both of which were clinically active, and very large quantities of immunoreactive gastrins, which were biologically active but clinically silent (normal gastric acid secretion and no peptic ulceration). The presence of parietal cell antibodies, with no increase in the plasma concentrations of hormones which can inhibit gastric acid secretion (secretin, GIP and VIP), suggests that many of the of the parietal cells may have been blocked by the autoantibodies.
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PMID:Clinically silent gross hypergastrinaemia from a multiple hormone-secreting pancreatic apudoma. 20 4

Recent data on the immunolocalization of regulatory peptides and related propeptide sequences in endocrine cells and tumors of the gastrointestinal tract, pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptides are the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, alpha-MSH and CLIP (corticotropin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenaline-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.
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PMID:Endocrine cells producing regulatory peptides. 329 70

Physiological regulatory mechanisms of gastric acid secretion are the basis for all those studies which attempt to analyze the pathophysiological role of acid secretion. The major stimulus of parietal cell function is food intake which acts via activation of cephalic-vagal and gastric mechanisms. Cephalic phase of acid secretion is augmented predominantly by acetylcholine and gastrin while histamine is of major importance during the gastric phase. A contribution of neuropeptides located in the ex- and intrinsic nervous system such as enkephalin, beta-endorphin, gastrin-releasing peptide and neuromedin C ist most likely, however, their exact physiological role remains to be determined especially in man. Following maximal acid secretion parietal cell function is turned down which is paralleled by the decrease of intragastric pH. The mechanisms responsible for this effect originate in the stomach and small intestine. In contrast to the stimulatory factors the physiologically relevant inhibitors of acid secretion are less well known. Hormones such as somatostatin, glucagon-like peptide-1 (7-36)-NH2 and peptide YY are presumably of importance. The role of secretin, GIP, CCK and neurotensin is somewhat more controversial and remains to be examined in greater detail in humans. Especially the synergistic action of gastrointestinal hormones is virtually unknown. The increasing knowledge of the complex regulatory mechanisms in the stomach should result in new perspectives for the pathogenesis of peptic ulcer disease.
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PMID:[Physiologic regulation of gastric acid secretion]. 847 47

The diagnosis of Cushing's syndrome remains a challenge in clinical endocrinology. Cushing's syndromes are usually classified as dependent or independent from ACTH. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic CRH syndrome. These ACTH-dependent Cushing's syndromes usually present diffusely hyperplastic adrenal glands. In the second class, are cortisol producing unilateral adrenocortical adenomas or carcinomas. New entities have recently emerged as bilateral adrenal hyperplasia not dependent from ACTH; their etiopathogenies are heterogeneous with illicit expressions at the adrenal level of functional receptors to various ligands: GIP, catecholamines, lutropin... The knowledge of such entities has to be taken into consideration in the diagnostic and management of ACTH independent Cushing syndromes.
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PMID:[Cushing syndromes due to aberrant expression of functional receptors other than ACTH. A new organic hypercorticism syndrome entity]. 1124 1