The Effect of the Mammalian Neuropeptide, Gastrin-Releasing Peptide (GRP), on Gastrointestinal and Pancreatic Hormone Secretion in Man

1983 ◽  
Vol 65 (4) ◽  
pp. 365-371 ◽  
Author(s):  
Susan M. Wood ◽  
Roland T. Jung ◽  
Joan D. Webster ◽  
Mohammed A. Ghatei ◽  
Thomas E. Adrian ◽  
...  
Keyword(s):  
Hormone Secretion ◽  
Significant Elevation ◽  
Plasma Gastrin ◽  
Nerve Fibres ◽  
Selective Effect ◽  
Specific Location ◽  
Gastrin Releasing Peptide ◽  
Pancreatic Hormone ◽  
Mammalian Peptide ◽  
The Brain

1. Gastrin-releasing peptide, a newly isolated mammalian peptide similar in its structure and actions to the amphibian peptide, bombesin, has recently been localized to nerves in the brain, gut and pancreas. The present study investigates its effects on gut and pancreatic peptides in man. 2. Intravenous infusion of 0.7 and 2.9 pmol min−1 kg−1 produced significant elevation of plasma gastrin, cholecystokinin-like immuno- reactivity and neurotensin. It was found also to potentiate glucose-dependent insulin secretion. 3. Its specific location in nerve fibres in the proximal gut and pancreas and its selective effect on gastroenteropancreatic peptides may favour its role as a physiological regulatory neuropeptide.

Liver glycogen-induced enhancements in hypoglycemic counterregulation require neuroglucopenia.

2021 ◽  
Author(s):  
Shana O Warner ◽  
Abby M Wadian ◽  
Marta S. Smith ◽  
Ben Farmer ◽  
Yufei Dai ◽  
...  
Keyword(s):  
Glycogen Content ◽  
Hormone Secretion ◽  
Control Period ◽  
Liver Glycogen ◽  
Saline Infusion ◽  
Glucose Levels ◽  
Liver Glycogen Content ◽  
Patients With Diabetes ◽  
Arterial Plasma ◽  
The Brain

Iatrogenic hypoglycemia is a prominent barrier to achieving optimal glycemic control in patients with diabetes, in part due to dampened counterregulatory hormone responses. It has been demonstrated that elevated liver glycogen content can enhance these hormonal responses through signaling to the brain via afferent nerves, but the role that hypoglycemia in the brain plays in this liver glycogen effect remains unclear. During the first 4hrs of each study, the liver glycogen content of dogs was increased by using an intraportal infusion of fructose to stimulate hepatic glucose uptake (HG; n=13), or glycogen was maintained near fasting levels with a saline infusion (NG; n=6). After a 2hr control period, during which the fructose/saline infusion was discontinued, insulin was infused intravenously for an additional 2hrs to bring about systemic hypoglycemia in all animals, whereas brain euglycemia was maintained in a subset of the HG group by infusing glucose bilaterally into the carotid and vertebral arteries (HG-HeadEu; n=7). Liver glycogen content was markedly elevated in the two HG groups (43±4, 73±3 and 75±7 mg/g in NG, HG and HG-HeadEu, respectively). During the hypoglycemic period, arterial plasma glucose levels were indistinguishable between groups (53±2, 52±1 and 51±1 mg/dL, respectively), but jugular vein glucose levels were kept euglycemic (88±5 mg/dL) only in the HG-HeadEu group. Glucagon and epinephrine responses to hypoglycemia were higher in HG compared to NG, whereas despite the increase in liver glycogen, neither increased above basal in HG-HeadEu. These data demonstrate that the enhanced counterregulatory hormone secretion that accompanies increased liver glycogen content requires hypoglycemia in the brain.

scholarly journals A selective effect of dopamine on information-seeking

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Valentina Vellani ◽  
Lianne P de Vries ◽  
Anne Gaule ◽  
Tali Sharot
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Information Seeking ◽  
Selective Effect ◽  
Reward Seeking ◽  
The Impact ◽  
The Brain ◽  
Insight Into ◽  
Primary Reward

Humans are motivated to seek information from their environment. How the brain motivates this behavior is unknown. One speculation is that the brain employs neuromodulatory systems implicated in primary reward-seeking, in particular dopamine, to instruct information-seeking. However, there has been no causal test for the role of dopamine in information-seeking. Here, we show that administration of a drug that enhances dopamine function (dihydroxy-L-phenylalanine; L-DOPA) reduces the impact of valence on information-seeking. Specifically, while participants under Placebo sought more information about potential gains than losses, under L-DOPA this difference was not observed. The results provide new insight into the neurobiology of information-seeking and generates the prediction that abnormal dopaminergic function (such as in Parkinson’s disease) will result in valence-dependent changes to information-seeking.

scholarly journals The gastrin releasing peptide, GRP, is differentially expressed in brain metastatic breast cancer.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Brain Metastasis ◽  
Microarray Data ◽  
Metastatic Breast ◽  
Metastatic Tumor ◽  
Clinical Problem ◽  
Primary Tumors ◽  
Gastrin Releasing Peptide ◽  
The Brain

Metastasis to the brain is a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to compare primary and metastatic tumor transcriptomes to discover genes associated with brain metastasis in patients with metastatic breast cancer. We found that the gastrin releasing peptide, encoded by GRP, was among the genes whose expression was most different in the brain metastases of patients with metastatic breast cancer as compared to primary tumors of the breast. Molecular functions of gastrin releasing peptide may be relevant to the processes by which tumor cells of the breast metastasize to the breast. Down-regulation of GRP may be an important event for metastasis of primary tumor-derived cancer cells to the brain in humans with metastatic breast cancer.

Concurrent elevation of fundic somatostatin prevents gastrin stimulation by GRP

1999 ◽  
Vol 276 (1) ◽  
pp. G21-G27 ◽  
Author(s):  
Yana Zavros ◽  
William R. Fleming ◽  
Arthur Shulkes
Keyword(s):  
Normal Animal ◽  
Differential Regulation ◽  
Local Source ◽  
Major Influence ◽  
Plasma Gastrin ◽  
Gastrin Releasing Peptide ◽  
Gastrin Secretion ◽  
Stimulation Of

Gastrin-releasing peptide (GRP) can stimulate both gastrin and somatostatin (SOM) secretion, but, as gastrin increases SOM and SOM in turn inhibits gastrin, the overall endpoint in terms of gastrin output is variable. To examine the mechanisms involved, we compared the effects of GRP on gastrin secretion in normal sheep and sheep chronically immunized against SOM. In the normal animal, GRP had no effect on either plasma gastrin or SOM. However, in sheep immunized against SOM, GRP stimulated gastrin secretion, suggesting that the concurrent stimulation of SOM prevents the increase in gastrin secretion. To determine the local source of SOM, GRP was then infused into nonimmunized sheep with cannulas draining blood from the fundus and antrum. GRP stimulated fundic SOM output but inhibited antral SOM and gastrin secretion, demonstrating that the fundus was the source of the SOM. Because cholinergic interactions have a major influence on the effects of GRP, a cholinergic stimulus was administered, and we found that the responses were different: SOM output was inhibited in both the antrum and fundus, and antral gastrin secretion was increased. The present study demonstrates two further instances of the differential regulation of SOM from the antrum and fundus. GRP fails to stimulate gastrin because of an increase in fundic SOM, whereas gastrin levels increase following a cholinergic stimulus because of inhibition of both antral and fundic SOM secretion.

CSF Monoamines in Autistic Syndromes and Other Pervasive Developmental Disorders of Early Childhood

1987 ◽  
Vol 151 (1) ◽  
pp. 89-94 ◽  
Author(s):  
C. Gillberg ◽  
L Svennerholm
Keyword(s):  
Neurodevelopmental Disorders ◽  
Pervasive Developmental Disorders ◽  
Developmental Disorders ◽  
Homovanillic Acid ◽  
Monoamine Metabolites ◽  
Autistic Children ◽  
Nerve Fibres ◽  
Normal Children ◽  
The Brain ◽  
Childhood Psychoses

Spinal fluid concentrations of the three major monoamine metabolites were examined in 25 infantile autistic children and 12 children with other childhood psychoses, and were contrasted with results obtained in normal children and in groups of children with neurological and neurodevelopmental disorders. Autistic children showed absolute and relative increases of the dopamine metabolite homovanillic acid. The group with other childhood psychoses also showed an increase in HVA level; in this group there were also indications of high levels of serotonin and norepinephrine metabolites. The results are discussed in the context of a pathogenetic model for autism involving hyperfunction of dopaminergic nerve fibres in the brain stem-mesolimbic system.

scholarly journals Arginine-induced pancreatic hormone secretion during exercise in rats

1996 ◽  
Vol 81 (6) ◽  
pp. 2528-2533 ◽  
Author(s):  
Fethi Trabelsi ◽  
Jean-Marc Lavoie
Keyword(s):  
Hormone Secretion ◽  
Exercise Bout ◽  
Glucagon Secretion ◽  
Sympathoadrenal System ◽  
Control Groups ◽  
Insulin And Glucagon Secretion ◽  
Hormone Responses ◽  
Pancreatic Hormone ◽  
Hepatic Branch

Trabelsi, Fethi, and Jean-Marc Lavoie. Arginine-induced pancreatic hormone secretion during exercise in rats. J. Appl. Physiol. 81(6): 2528–2533, 1996.—The aim of the present investigation was to 1) determine whether arginine-induced pancreatic hormone secretion can be modified during an exercise bout, and 2) verify whether the sectioning of the hepatic branch of the vagus nerve can alter the arginine-induced insulin and glucagon secretion during exercise in rats. To this end, we studied the effects of an intraperitoneal injection of arginine (1 g/kg body mass) during an exercise bout (30 min, 26 m/min, 0% grade) on the pancreatic hormone responses. These effects were determined in one group of sham-operated exercising rats and compared with three control groups: one group of resting rats, one group of saline-injected exercising rats, and one group of hepatic-vagotomized exercising rats. Five minutes after the injection of arginine, significant ( P < 0.05) increases in insulin, glucagon, and C-peptide concentrations were observed in exercising as well as in resting rats. These responses were not, however, altered by the hepatic vagotomy and/or by the exercise bout. It is concluded that arginine is a potent stimulus of pancreatic hormone secretion during exercise, even though the sympathoadrenal system is activated. These results also indicate that a hepatic vagotomy does not seem to influence arginine-induced hormonal pancreatic responses and question the role of the putative hepatic arginoreceptors in the control of the pancreatic hormone secretion during exercise.

Nonadrenergic sympathetic neural influences on basal pancreatic hormone secretion

1988 ◽  
Vol 255 (6) ◽  
pp. E785-E792 ◽  
Author(s):  
B. E. Dunning ◽  
B. Ahren ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Hormone Secretion ◽  
Immunoreactive Insulin ◽  
High Dose ◽  
Adrenergic Blockade ◽  
Islet Hormone ◽  
Anesthetized Dogs ◽  
Adrenergic Antagonists ◽  
Induced Changes ◽  
Pancreatic Hormone ◽  
Neural Influences

Evidence for peptidergic innervation of the islets of Langerhans is increasing, yet the role of neuropeptides in mediating neurally induced changes of islet function is not clear. To determine if nonadrenergic transmitters make an important contribution to sympathetic neural effects on basal pancreatic hormone secretion, we examined the effect of local sympathetic nerve stimulation (SNS) on the output of immunoreactive insulin (IRI), immunoreactive glucagon (IRG), and somatostatin (SLI) from the duodenal lobe of the pancreas in situ in halothane-anesthetized dogs, under conditions where the actions of the classical transmitter norepinephrine (NE) should be blocked by propranolol (PROP) and yohimbine (YO). In the absence of adrenergic antagonists, SNS rapidly reduced the output of IRI (delta = -1.34 +/- 0.91 mU/min) and SLI (delta = -600 +/- 350 fmol/min) and stimulated that of IRG (delta = +1.39 +/- 0.57 ng/min). In the presence of PROP and YO, SNS induced similar changes of hormone secretion: delta IRI, -1.30 +/- 0.53 mU/min; delta SLI, -480 +/- 180 fmol/min; delta IRG = +1.89 +/- 0.63 ng/min. Because PROP and YO abolished the pancreatic effects of high dose infusions of NE (1 microgram.kg-1.min-1 iv), we suggest that the antagonists produced sufficient, combined adrenergic blockade at the level of the islet, and we conclude that a nonadrenergic neurotransmitter or modulator plays a major role in mediating sympathetic neural effects on basal islet hormone secretion.

CELLULAR LOCALIZATION OF A PROLACTIN-LIKE ANTIGEN IN THE RAT BRAIN

1979 ◽  
Vol 83 (2) ◽  
pp. 261-NP ◽  
Author(s):  
G. TOUBEAU ◽  
J. DESCLIN ◽  
M. PARMENTIER ◽  
J. L. PASTEELS
Keyword(s):  
Rat Brain ◽  
Cellular Localization ◽  
Female Rats ◽  
Nerve Fibres ◽  
Male And Female ◽  
Immunoreactive Material ◽  
Paraventricular Nuclei ◽  
Male And Female Rats ◽  
The Brain

The distribution of immunoreactive neurones and fibres was studied in rat brain using an antiserum to rat prolactin. Neurones containing the immunoreactive material were localized in the arcuate, ventromedial, premamillary, supraoptic and paraventricular nuclei of the hypothalamus. Immunoreactive nerve fibres were widely distributed within the brain. No differences were observed in labelling between male and female rats, or as a consequence of hypophysectomy.

Evidence that endogenous GRP in rat stomach mediates omeprazole-induced hypergastrinemia

1996 ◽  
Vol 271 (5) ◽  
pp. G799-G804 ◽  
Author(s):  
Y. Takehara ◽  
K. Sumii ◽  
A. Tari ◽  
M. Yoshihara ◽  
M. Sumii ◽  
...  
Keyword(s):  
Methyl Ester ◽  
Serum Gastrin ◽  
Physiological Role ◽  
Gastrin Release ◽  
Intragastric Ph ◽  
Significant Elevation ◽  
Rat Stomach ◽  
Gastrin Releasing Peptide ◽  
Bombesin Antagonist

To investigate the physiological role of endogenous gastrin-releasing peptide (GRP) in regulating the release of gastrin, we evaluated the response of intragastric pH, gastrin, and GRP after omeprazole treatment in rats. A significant elevation of the plasma level of GRP (P< 0.01) and a significant reduction of the antral content of GRP (P <0.05) were observed after the administration of 100 mg/kg omeprazole. The antral content of GRP was significantly decreased 12 h after omeprazole administration and thereafter gradually returned to control levels. Peak values for intragastric pH and plasma GRP were observed 3 h after omeprazole administration and before the peak of serum gastrin. The bombesin antagonist [D-Phe6]-bombesin-(6,13)-methyl ester significantly inhibited gastrin release after omeprazole treatment (P < 0.05). These observations indicate that omeprazole-induced inhibition of acid secretion stimulates the release of GRP and suggest that the secretion of GRP induced by omeprazole may stimulate the secretion of gastrin, at least in the early phase.

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