Gastrin Detects Specificity: Analytical Big Reactivity with 7% Cross (G17); React Not Cross (G34); Does Gastrin with G13

Total Page：16

File Type：pdf, Size：1020Kb

Gastrin Detects Specificity: Analytical Big Reactivity with 7% Cross (G17); React Not Cross (G34); Does Gastrin with G13

Gastrin 478X Clinical Use Clinical Background • Diagnose gastrinoma Gastrin is a polypeptide hormone • Differential diagnosis of peptic ulcer secreted by the G cells of the gastric antral mucosa and proximal duodenal disease and gastrin-secreting tumors Test Alphabetical cells. Gastrin is a potent stimulator of Reference Range antral acid secretion, and also has Section pg/mL trophic actions on the parietal cells, Adults <100 chief cells, and enterochromaffin-like cells in the oxyntic mucosa. Gastrin Children levels increase with food intake 5-7 y 13-64 (protein, amino acids) and age. Levels decrease with gastric acid Interpretive Information secretion. • Gastrinoma In Zollinger-Ellison syndrome (ZE • Pernicious anemia syndrome), a pancreatic neoplasm produces large amounts of gastrin, • Atrophic gastritis with anacidity which in turn stimulates excess gastric Zollinger-Ellison syndrome: gastrin acid secretion and peptic ulcer disease. levels >200 pg/mL (Roy PK, et al. A variety of pathological, but non- Medicine. 2000;79:379-411.) tumorous, disorders in which gastric acid secretion is low also lead to ®’ ®’ Zantac , Prilosec , and pepsid elevations in blood gastrin; these interfere with gastrin production. disorders include pernicious anemia and atrophic gastritis with anacidity. Secretin- or calcium-stimulation tests can assist in differentiating tumors from gastrin secreted by the antrum in patients with slight or moderate hypergastrinemia. Method • Immunochemiluminometric assay (ICMA) • Analytical sensitivity: 10 pg/mL • Analytical specificity: detects gastrin (G17); 7% cross reactivity with big gastrin (G34); does not cross react with G13. Specimen Requirements 1 mL frozen serum 0.5 mL minimum No additive red top preferred SST red top acceptable Overnight fasting is required. 81.

Copy Link

Recommended publications

Coffee and Its Effect on Digestion
Expert report Coffee and its effect on digestion By Dr. Carlo La Vecchia, Professor of Medical Statistics and Epidemiology, Dept. of Clinical Sciences and Community Health, Università degli Studi di Milano, Italy. Contents 1 Overview 2 2 Coffee, a diet staple for millions 3 3 What effect can coffee have on the stomach? 4 4 Can coffee trigger heartburn or GORD? 5 5 Is coffee associated with the development of gastric or duodenal ulcers? 6 6 Can coffee help gallbladder or pancreatic function? 7 7 Does coffee consumption have an impact on the lower digestive tract? 8 8 Coffee and gut microbiota — an emerging area of research 9 9 About ISIC 10 10 References 11 www.coffeeandhealth.org May 2020 1 Expert report Coffee and its effect on digestion Overview There have been a number of studies published on coffee and its effect on different areas of digestion; some reporting favourable effects, while other studies report fewer positive effects. This report provides an overview of this body of research, highlighting a number of interesting findings that have emerged to date. Digestion is the breakdown of food and drink, which occurs through the synchronised function of several organs. It is coordinated by the nervous system and a number of different hormones, and can be impacted by a number of external factors. Coffee has been suggested as a trigger for some common digestive complaints from stomach ache and heartburn, through to bowel problems. Research suggests that coffee consumption can stimulate gastric, bile and pancreatic secretions, all of which play important roles in the overall process of digestion1–6.
[Show full text]
Regulation of the Gastrin Promoter by Epidermal Growth Factor and Neuropeptides JUANITA M
Proc. Nati. Acad. Sci. USA Vol. 86, pp. 3036-3040, May 1989 Biochemistry Regulation of the gastrin promoter by epidermal growth factor and neuropeptides JUANITA M. GODLEY AND STEPHEN J. BRAND Gastrointestinal Unit, Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114 Communicated by Kurt J. Isselbacher, December 30, 1988 ABSTRACT The regulation of gastrin gene transcription gastrin secretion (12, 13), the effect of GRP on gastrin gene was studied in GH4 pituitary cells transfected with constructs expression has not been reported. Antral G cells are also comprised of the first exon of the human gastrin gene and inhibited by the paracrine release of somatostatin from various lengths of 5' regulatory sequences ligated upstream of adjacent antral D cells (14), and local release of somatostatin the reporter gene chloramphenicol acetyltransferase. Gastrin inhibits gastrin gene expression as well as gastrin secretion reporter gene activity in GH4 cells was equal to the activity of (15). a reporter gene transcribed from the endogenously expressed In contrast to the detailed studies on gastrin secretion, the growth hormone promoter. The effect of a variety of peptides regulation of gastrin gene expression has not been well on gastrin gene transcription including epidermal growth investigated. The cellular mechanisms controlling gastrin factor (normally present in the gastric lumen), gastrin- secretion have been analyzed using isolated primary G cells releasing peptide, vasoactive intestinal peptide, and somato- (12, 13); however, the limited viability of these cells has statin (present in gastric nerves) was assessed. Epidermal precluded their use in studying the regulation of gastrin gene growth factor increased the rate ofgastrin transcription almost transcription using DNA transfection techniques.
[Show full text]
Adrenocorticotrophic and Melanocyte-Stimulating Peptides in the Human Pituitary by ALEXANDER P
Biochem. J. (1974) 139, 593-602 593 Printed in Great Britain Adrenocorticotrophic and Melanocyte-Stimulating Peptides in the Human Pituitary By ALEXANDER P. SCOTT and PHILIP J. LOWRY* Department ofChemical Pathology, St. Bartholomew's Hospital, London EC1A 7BE, U.K. and CIBA Laboratories, Horsham, Sussex RH12 4AB, U.K. (Received 7 December 1973) The adrenocorticotrophic and melanocyte-stimulating peptides of the human pituitary were investigated by means of radioimmunoassay, bioassay and physicochemical pro- cedures. Substantial amounts of adrenocorticotrophin and a peptide resembling /8-lipotrophin were identified in pituitary extracts, but a-melanocyte-stimulating hormone, ,B-melanocyte-stimulating hormone and corticotrophin-like intermediate lobe peptide, which have been identified in thepars intermedia ofpituitaries from other vertebrates, were not found. The absence of fJ-melanocyte-stimulating hormone appears to contradict previous chemical and radioimmunological studies. Our results suggest, however, that it is not a natural pituitary peptide but an artefact formed by enzymic degradation of ,6-lipotrophin during extraction. Melanocyte-stimulating and corticotrophic pep- extraction of human pituitaries for growth hormone tides have been identified in the pituitaries of all (Dixon, 1960). Its stucture was determined by Harris vertebrate species studied, and several have been (1959) and shown to be similar to ,B-MSH isolated isolated and characterized. They belong to two from other species, except for the presence of an structually related classes, namely those related to extra four amino acids at the N-terminus. The adrenocorticotrophin (ACTH) including ACTH, presence of sufficient amounts of 8-MSH in human a-melanocyte-stimulating hormone (a-MSH) and pituitaries to account alone for the bulk of the 'corticotrophin-like intermediate lobepeptide' ACTH melanocyte-stimulating activity in the pituitary (18-39) peptide (CLIP), and others related to fi- extracts was shown by radioimmunoassay (Abe et al., melanocyte-stimulating hormone (,B-MSH) including 1967b).
[Show full text]
Expression and Localization of Gastrin Messenger RNA and Peptide in Spermatogenic Cells
Expression and localization of gastrin messenger RNA and peptide in spermatogenic cells. M Schalling, … , T Hökfelt, J F Rehfeld J Clin Invest. 1990;86(2):660-669. https://doi.org/10.1172/JCI114758. Research Article In previous studies we have shown that the gene encoding cholecystokinin (CCK) is expressed in spermatogenic cells of several mammalian species. In the present study we show that a gene homologous to the CCK-related hormone, gastrin, is expressed in the human testis. The mRNA hybridizing to a human gastrin cDNA probe in the human testis was of the same size (0.7 kb) as gastrin mRNA in the human antrum. By in situ hybridization the gastrinlike mRNA was localized to seminiferous tubules. Immunocytochemical staining of human testis revealed gastrinlike peptides in the seminiferous tubules primarily at a position corresponding to spermatids and spermatozoa. In ejaculated spermatozoa gastrinlike immunoreactivity was localized to the acrosome. Acrosomal localization could also be shown in spermatids with electron microscopy. Extracts of the human testis contained significant amounts of progastrin, but no bioactive amidated gastrins. In contrast, ejaculated sperm contained mature carboxyamidated gastrin 34 and gastrin 17. The concentration of gastrin in ejaculated human spermatozoa varied considerably between individuals. We suggest that amidated gastrin (in humans) and CCK (in other mammals) are released during the acrosome reaction and that they may be important for fertilization. Find the latest version: https://jci.me/114758/pdf Expression and Localization of Gastrin Messenger RNA and Peptide in Spermatogenic Cells Martin Schalling,* Hhkan Persson,t Markku Pelto-Huikko,*9 Lars Odum,1I Peter Ekman,I Christer Gottlieb,** Tomas Hokfelt,* and Jens F.
[Show full text]
Supplementary Table 1. Clinico-Pathologic Features of Patients with Pancreatic Neuroendocrine Tumors Associated with Cushing’S Syndrome
Supplementary Table 1. Clinico-pathologic features of patients with pancreatic neuroendocrine tumors associated with Cushing’s syndrome. Review of the English/Spanish literature. Other hormones Age of Cortisol Other hormones Other ACTH Size (ICH or assay) ENETS Follow- Time Year Author Sex CS onset level (Blood syndromes or Site MET Type AH level (cm) corticotrophic Stage up (months) (years) (µg/dl) detection) NF other differentiation 1 1 1946 Crooke F 28 uk uk none no 4.5 H liver/peritoneum NET uk uk yes IV DOD 6 2 1956 Rosenberg 2 F 40 uk 92 none no 10 B liver NET uk uk yes IV PD 3 & p 3 1959 Balls F 36 uk elevated insulin Insulinoma 20 B liver/LNl/lung NET uk uk yes IV DOD 1 4 & 4 1962 Meador F 47 13~ elevated none no uk T liver/spleen NET ACTH uk yes IV uk 5 1963 Liddle5 uk uk uk elevated uk uk uk uk uk NET ACTH uk uk uk uk 6 1964 Hallwright6 F 32 uk uk none no large H LN/liver NET ACTH, MSH uk yes IV DOD 24 7 1965 Marks7 M 43 uk elevated insulin insulinomas 1.8 T liver NET uk uk yes IV DOD 7 8 1965 Sayle8 F 62 uk uk none carcinoidb 4 H LN/liver NET uk uk yes IV DOD 6 9 1965 Sayle8 F 15 uk uk none no 4 T no NET ACTH uk yes IIa DOD 5 9 b mesentery/ 10 1965 Geokas M 59 uk uk gastrin ZES large T NET uk uk yes IV DOD 2 LN/pleural/bone 11 1965 Law10 F 35 1.2 ∞ 91 gastrin ZESs uk B LN/liver NET ACTH, MSH gastrin yes IV PD 12 1967 Burkinshaw11 M 2 uk 72 none no large T no NET uk uk no uk AFD 12 13 1968 Uei12 F 9 uk uk none ZESs 7 T liver NET ACTH uk yes IV DOD 8 13 PTH, ADH, b gastrin, 14 1968 O'Neal F 52 13~ uk ZES uk T LN/liver/bone NET
[Show full text]
Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide
Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide MARK FELDMAN, CHARLES T. RICHARDSON, IAN L. TAYLOR, and JOHN H. WALSH, Departments of Internal Medicine, Veterans Administration Hospital, Dallas, Texas 75216; University of California at Los Angeles Health Science Center, Los Angeles, California 90093; and The University of Texas Health Science Center at Dallas, Southwestern Medical School, Dallas, Texas 75235 A B S TRA C T We studied the effect of several doses of the rise in serum gastrin concentration induced by in- atropine on the serum gastrin and pancreatic poly- sulin hypoglycemia was further increased by atropine peptide responses to vagal stimulation in healthy premedication (1). In addition, several workers have human subjects. Vagal stimulation was induced by shown that atropine increases the serum gastrin con- sham feeding. To eliminate the effect of gastric acidity centration after an eaten meal (2-4). These observa- on gastrin release, gastric pH was held constant (pH 5) tions, together with the fact that basal and postprandial and acid secretion was measured by intragastric titra- gastrin levels rise after vagotomy (5-7), have led to tion. Although a small dose of atropine (2.3 ,ug/kg) speculation that the vagus nerve can inhibit, as well as significantly inhibited the acid secretory response and stimulate, gastrin release. completely abolished the pancreatic polypeptide re- For several reasons, however, none of these observa- sponse to sham feeding, this dose of atropine signifi- tions proves that the vagus nerve actually inhibits cantly enhanced the gastrin response. Higher atropine gastrin release under normal circumstances. First, doses (7.0 and 21.0,g/kg) had effects on gastrin and studies using insulin hypoglycemia as a vagal stimulant pancreatic polypeptide release which were similar to must be interpreted with caution because there is the 2.3-pAg/kg dose.
[Show full text]
Adipose Tissue As an Endocrine Organ
0021-972X/04/$15.00/0 The Journal of Clinical Endocrinology & Metabolism 89(6):2548–2556 Printed in U.S.A. Copyright © 2004 by The Endocrine Society doi: 10.1210/jc.2004-0395 Adipose Tissue as an Endocrine Organ ERIN E. KERSHAW AND JEFFREY S. FLIER Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215 Adipose tissue is a complex, essential, and highly active met- the renin-angiotensin system, and resistin. Adipose tissue is abolic and endocrine organ. Besides adipocytes, adipose tis- also a major site for metabolism of sex steroids and glucocor- Downloaded from https://academic.oup.com/jcem/article-abstract/89/6/2548/2870285 by guest on 09 April 2020 sue contains connective tissue matrix, nerve tissue, stromo- ticoids. The important endocrine function of adipose tissue is vascular cells, and immune cells. Together these components emphasized by the adverse metabolic consequences of both function as an integrated unit. Adipose tissue not only re- adipose tissue excess and deficiency. A better understanding sponds to afferent signals from traditional hormone systems of the endocrine function of adipose tissue will likely lead to and the central nervous system but also expresses and se- more rational therapy for these increasingly prevalent disor- cretes factors with important endocrine functions. These fac- ders. This review presents an overview of the endocrine func- tors include leptin, other cytokines, adiponectin, complement tions of adipose tissue. (J Clin Endocrinol Metab 89: 2548–2556, components, plasminogen activator inhibitor-1, proteins of 2004) HE TRADITIONAL VIEW of adipose tissue as a passive states (4).
[Show full text]
Somatostatin Inhibits Gastric Acid Secretion After Gastric Mucosal Prostaglandin Synthesis Inhibition by Indomethacin in Man
Gut: first published as 10.1136/gut.26.11.1189 on 1 November 1985. Downloaded from Gut, 1985, 26, 1189-1191 Somatostatin inhibits gastric acid secretion after gastric mucosal prostaglandin synthesis inhibition by indomethacin in man M H MOGARD, V MAXWELL, T KOVACS, G VAN DEVENTER, J D ELASHOFF, T YAMADA, G L KAUFFMAN JR, AND J H WALSH From the Centerfor Ulcer Research and Education, VA Wadsworth MedicallSurgical Services and UCLA, LosAngeles, California, USA. SUMMARY The inhibitory effect of indomethacin, 200+200 mg administered per os over 24 hours, on the prostaglandin E2 generative capacity of gastric mucosal tissue was determined in healthy male volunteers. The effect of prostaglandin synthesis inhibition on somatostatin induced suppression of food-stimulated acid secretion was tested. Peptone meal stimulated acid secretion was quantified in five healthy volunteers by intragastric titration with and without indomethacin pretreatment. Somatostatin doses of 200, 400, and 800 pmol/kg/h each significantly inhibited the peptone stimulated acid output. Indomethacin treatment, resulting in 90% inhibition of prostaglandin E2 synthesis, did not affect glucose- or peptone-stimulated acid output or modify the inhibitory action of somatostatin. Clinically, acid inhibition by somatostatin has been used to treat bleeding peptic ulcers. Ulcer haemorrhage may be preceded by an excessive use of drugs that inhibit prostaglandin synthesis such as aspirin or other non-steroidal anti-inflammatory agents. Recent observations in the rat indicate that prostaglandins mediate the inhibitory action of somatostatin on gastric acid secretion. The present results suggest that prostaglandins are not http://gut.bmj.com/ required for inhibition of gastric acid secretion by somatostatin in man.
[Show full text]
The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation
biomedicines Review The Role of Corticotropin-Releasing Hormone at Peripheral Nociceptors: Implications for Pain Modulation Haiyan Zheng 1, Ji Yeon Lim 1, Jae Young Seong 1 and Sun Wook Hwang 1,2,* 1 Department of Biomedical Sciences, College of Medicine, Korea University, Seoul 02841, Korea; [email protected] (H.Z.); [email protected] (J.Y.L.); [email protected] (J.Y.S.) 2 Department of Physiology, College of Medicine, Korea University, Seoul 02841, Korea * Correspondence: [email protected]; Tel.: +82-2-2286-1204; Fax: +82-2-925-5492 Received: 12 November 2020; Accepted: 15 December 2020; Published: 17 December 2020 Abstract: Peripheral nociceptors and their synaptic partners utilize neuropeptides for signal transmission. Such communication tunes the excitatory and inhibitory function of nociceptor-based circuits, eventually contributing to pain modulation. Corticotropin-releasing hormone (CRH) is the initiator hormone for the conventional hypothalamic-pituitary-adrenal axis, preparing our body for stress insults. Although knowledge of the expression and functional proﬁles of CRH and its receptors and the outcomes of their interactions has been actively accumulating for many brain regions, those for nociceptors are still under gradual investigation. Currently, based on the evidence of their expressions in nociceptors and their neighboring components, several hypotheses for possible pain modulations are emerging. Here we overview the historical attention to CRH and its receptors on the peripheral nociception and the recent increases in information regarding their roles in tuning pain signals. We also brieﬂy contemplate the possibility that the stress-response paradigm can be locally intrapolated into intercellular communication that is driven by nociceptor neurons.
[Show full text]
Reciprocal Regulation of Antral Gastrin and Somatostatin Gene Expression by Omeprazole-Induced Achlorhydria
Reciprocal regulation of antral gastrin and somatostatin gene expression by omeprazole-induced achlorhydria. S J Brand, D Stone J Clin Invest. 1988;82(3):1059-1066. https://doi.org/10.1172/JCI113662. Research Article Gastric acid exerts a feedback inhibition on the secretion of gastrin from antral G cells. This study examines whether gastrin gene expression is also regulated by changes in gastric pH. Achlorhydria was induced in rats by the gastric H+/K+ ATPase inhibitor, omeprazole (100 mumol/kg). This resulted in fourfold increases in both serum gastrin (within 2 h) and gastrin mRNA levels (after 24 h). Antral somatostatin D cells probably act as chemoreceptors for gastric acid to mediate a paracrine inhibition on gastrin secretion from adjacent G cells. Omeprazole-induced achlorhydria reduced D-cell activity as shown by a threefold decrease in antral somatostatin mRNA levels that began after 24 h. Exogenous administration of the somatostatin analogue SMS 201-995 (10 micrograms/kg) prevented both the hypergastrinemia and the increase in gastrin mRNA levels caused by omeprazole-induced achlorhydria. Exogenous somatostatin, however, did not influence the decrease in antral somatostatin mRNA levels seen with achlorhydria. These data, therefore, support the hypothesis that antral D cells act as chemoreceptors for changes in gastric pH, and modulates somatostatin secretion and synthesis to mediate a paracrine inhibition on gastrin gene expression in adjacent G cells. Find the latest version: https://jci.me/113662/pdf Reciprocal Regulation of Antral Gastrin and Somatostatin Gene Expression by Omeprazole-induced Achlorhydria Stephen J. Brand and Deborah Stone Departments ofMedicine, Harvard Medical School and Massachusetts General Hospital, Gastrointestinal Unit, Boston, Massachusetts Abstract Substantial evidence supports the hypothesis that gastric acid inhibits gastrin secretion through somatostatin released Gastric acid exerts a feedback inhibition on the secretion of from antral D cells (9, 10).
[Show full text]
Lecture Series Gastrointestinal Tract
Lecture series Gastrointestinal tract Professor Shraddha Singh, Department of Physiology, KGMU, Lucknow INNERVATION OF GIT • 1.Intrinsic innervation-1.Myenteric/Auerbach or plexus Local 2.Submucosal/Meissners plexus 2.Extrinsic innervation-1.Parasympathetic or -2.Sympathetic Higher centre Enteric Nervous System - Lies in the wall of the gut, beginning in the esophagus and - extending all the way to the anus - controlling gastrointestinal movements and secretion. - (1) an outer plexus lying between the longitudinal and circular muscle layers, called the myenteric plexus or Auerbach’s plexus, - controls mainly the gastrointestinal movements - (2) an inner plexus, called the submucosal plexus or Meissner’s plexus, that lies in the submucosa. - controls mainly gastrointestinal secretion and local blood flow Enteric Nervous System - The myenteric plexus consists mostly of a linear chain of many interconnecting neurons that extends the entire length of the GIT - When this plexus is stimulated, its principal effects are - (1) increased tonic contraction, or “tone,” of the gut wall, - (2) increased intensity of the rhythmical contractions, - (3) slightly increased rate of the rhythmical contraction, - (4) increased velocity of conduction of excitatory waves along the gut wall, causing more rapid movement of the gut peristaltic waves. - Inhibitory transmitter - vasoactive intestinal polypeptide (VIP) - pyloric sphincter, sphincter of the ileocecal valve Enteric Nervous System - The submucosal plexus is mainly concerned with controlling function within the inner wall - local intestinal secretion, local absorption, and local contraction of the submucosal muscle - Neurotransmitters: - (1) Ach (7) substance P - (2) NE (8) VIP - (3)ATP (9) somatostatin - (4) 5 – HT (10) bombesin - (5) dopamine (11) metenkephalin - (6) cholecystokinin (12) leuenkephalin Higher centre innervation - the extrinsic sympathetic and parasympathetic fibers that connect to both the myenteric and submucosal plexuses.
[Show full text]
Maternal Smoking and Infantile Gastrointestinal Dysregulation: the Case of Colic
Maternal Smoking and Infantile Gastrointestinal Dysregulation: The Case of Colic Edmond D. Shenassa, ScD*‡, and Mary-Jean Brown, ScD, RN§ ABSTRACT. Background. Infants’ healthy growth intestinal motilin levels and (2) higher-than-average lev- and development are predicated, in part, on regular func- els of motilin are linked to elevated risks of IC. Although tioning of the gastrointestinal (GI) tract. In the first 6 these findings from disparate fields suggest a physio- months of life, infants typically double their birth logic mechanism linking maternal smoking with IC, the weights. During this period of intense growth, the GI entire chain of events has not been examined in a single tract needs to be highly active and to function optimally. cohort. A prospective study, begun in pregnancy and Identifying modifiable causes of GI tract dysregulation continuing through the first 4 months of life, could pro- is important for understanding the pathophysiologic pro- vide definitive evidence linking these disparate lines of cesses of such dysregulation, for identifying effective research. Key points for such a study are considered. and efficient interventions, and for developing early pre- Conclusions. New epidemiologic evidence suggests vention and health promotion strategies. One such mod- that exposure to cigarette smoke and its metabolites may ifiable cause seems to be maternal smoking, both during be linked to IC. Moreover, studies of the GI system and after pregnancy. provide corroborating evidence that suggests that (1) Purpose. This article brings together information that smoking is linked to increased plasma and intestinal strongly suggests that infants’ exposure to tobacco smoke motilin levels and (2) higher-than-average intestinal mo- is linked to elevated blood motilin levels, which in turn tilin levels are linked to elevated risks of IC.
[Show full text]