Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine cells in the gastrointestinal tract of the domestic duck were identified immunocytochemically using antisera specific to bombesin, chromogranin A, cholecystokinin (CCK), gastrin, glucagon, neuron specific enolase (NSE), neurotensin, secretin, 5-hydroxytryptamine (5-HT), somatostatin, substance P and vasoactive intestinal polypeptide (VIP). Chromogranin A, 5-HT and somatostatin immunoreactive cells were widespread throughout the gastrointestinal tract. Bombesin immunoreactive cells were observed only in the proventriculus and the gizzard. CCK, substance P and neurotensin immunoreactive cells were present in the intestinal tracts from the duodenum to the colorectum. The latter were numerous also in the antrum. Gastrin cells were peculiar to the antrum but present also in the gizzard and small intestine. Glucagon immunoreactive cells were present in the jejunum-ileum and above all in the large intestine. Only few secretin cells were present in the duodenum. The highest frequency of endocrine cells was found in the antrum, while the lowest was observed in the caeca. Antisera to somatostatin and substance P showed numerous nerve cells and fibers besides endocrine cells, whereas NSE and VIP immunopositivity was found in the nervous structures only of the gut wall.
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PMID:An immunohistochemical study on the endocrine cells in the gastrointestinal tract of domestic duck. 168 96

The antagonistic effects of [D-Phe25]gastrin-releasing peptide (GRP)(18-27) and [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P (SP) on the stimulation of insulin release by GRP(18-27) from isolated canine pancreas were compared with that of [Ala23]GRP(18-27). The stimulation of insulin release by 1 nM GRP(18-27) was reduced to 24.1% and 15.4% by the prior infusion of 1 microM of [D-Arg1,D-Pro2,D-Trp7,9,Leu11]SP and 10 microM of [D-Phe25]GRP(18-27), respectively. Glucagon release by GRP(18-27) was not affected by these peptides using the above concentrations. The results indicate that these peptides are antagonists of bombesin-like peptide receptors on pancreatic B-cells, although the inhibitory activities are lower than that of [Ala23]GRP(18-27).
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PMID:Antagonism by GRP(18-27) and substance P analogues on insulin release stimulated by GRP(18-27). 169 92

An immunocytochemical investigation was carried out on round and spreading hemocytes of Planorbarius corneus by using 20 antisera to vertebrate bioactive peptides. The immunotests showed the presence of alpha 1-antichymotrypsin-bombesin-, calcitonin-, CCK-8 (INC)-, CCK-39-, gastrin-, glucagon-, Met-enkephalin-, neurotensin-, oxytocin-, somatostatin-, substance P-, VIP-, and vasopressin-immunoreactive molecules in the spreading hemocytes. The round hemocytes were only positive to anti-bombesin, anticalcitonin, anti-CCK-8 (INC), anti-CCK-39, anti-neurotensin, anti-oxytocin, anti-substance P and anti-vasopressin antibodies. No immunostaining was observed with anti-CCK-8 (Peninsula), anti-insulin, anti-prolactin, anti-thyroglobulin and anti-thyroxin (T4) antibodies. As probably in vertebrates, these bioactive peptides may modulate immuno cell function.
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PMID:Immunocytochemical evidence of vertebrate bioactive peptide-like molecules in the immuno cell types of the freshwater snail Planorbarius corneus (L.) (Gastropoda, Pulmonata). 169 11

Food intake can be increased or decreased after either central or peripheral administration of peptides. Galanin, neuropeptide Y, opioid peptides, growth-hormone-releasing hormone, and desacetyl-melanocyte stimulating hormone increase food intake whereas insulin, glucagon, cholecystokinin, anorectin, corticotropin-releasing hormone, neurotensin, bombesin, cyclo-his-pro, and thyrotropin-releasing hormone reduce food intake. Many of these peptides have reciprocal effects on food intake and sympathetic activity with those peptides that stimulate food intake reducing sympathetic activity and vice versa. In addition, neuropeptide Y specifically increases carbohydrate intake. Galanin and opioid peptides on the other hand increase fat intake whereas enterostatin reduces fat intake. Glucagon decreases protein intake. The effect of peptides on specific nutrients suggests that peptides may work in part by modulating basic feeding mechanisms to lead to the selection of specific nutrients from the diet. This hypothesis might be called a nutrient-specific model of peptide-induced food intake.
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PMID:Peptides affect the intake of specific nutrients and the sympathetic nervous system. 172 38

In the past 20 years, the mechanisms of the satiating effect of food that terminate a meal have been investigated intensively in rodents and in humans. This research has revealed that three peptides, cholecystokinin, pancreatic glucagon, and bombesin, released by ingested food from the gastrointestinal tract decrease meal size in a specific, dose-related manner without signs of acute toxicity or tolerance. In humans, the three peptides decrease meal size without decreasing the reported pleasure or satisfaction of the meal. Although their chemical structure and specific effect justify calling these peptides a new class of anorectic agents, not enough work has been done to evaluate their efficacy for weight loss in obese humans or their safety when administered for months.
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PMID:Are gut peptides a new class of anorectic agents? 172 40

The effect of bombesin against injury on rat islet B cells was studied in three kinds of experiments: (1). In vivo experiment, it was found that preinjection of bombesin (50 micrograms/kg, sublingual v.) could effectively prevent an increase of plasma glucose and decrease of plasma insulin in diabetic rat induced by alloxan (200 mg/kg, s.c.) (2). In vitro experiment, isolated pancreas perfusion showed that alloxan-induced (14 mmol/L) perfusion fluid inhibition of insulin secretion could be reversed by pretreatment of bombesin (10(-3) mmol/L). (3). Investigation on isolated and incubated islets demonstrated that alloxan induced decrease of insulin and somatostatin secretion and increase of glucagon secretion could be prevented by bombesin. The above-mentioned results suggest that bombesin may play an important role in the regulation of plasma glucose in diabetic rat and have a potent preventive effect against the development of diabetes.
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PMID:[Preventive effect of bombesin on alloxan-induced diabetes in rat]. 179 6

To determine whether CNS regulatory pathways are organized so that differential sympathetic outflow patterns occur in response to stress, we injected various doses of neostigmine or bombesin into the third cerebral ventricle of fed rats, and then measured the hepatic venous plasma concentrations of glucose, glucagon, insulin, and epinephrine. The following four groups of rats were studied. Group 1 was intact rats. Group 2 comprised intact rats receiving the constant infusion of a) somatostatin to inhibit the endogenous secretion of insulin and glucagon, and b) insulin to maintain the plasma insulin concentration at basal levels. The infusion was started from -30 minutes and given via a catheter in the femoral vein. Group 3 consisted of rats that underwent bilateral adrenal medullectomy (ADMX) one week before the experiment. Group 4 was ADMX rats administered a constant infusion of somatostain with insulin through a femoral vein, as above. The administration of 1 x 10(-9) mol neostigmine caused hepatic venous hyperglycemia mediated by three distinct pathways: 1) direct innervation of the liver, 2) a direct action of epinephrine on the liver, and 3) the action of glucagon on the liver. We estimated the relative contribution of these three factors to be about 47, 32, and 21%, respectively. Relative contributions of three factors of the doses of 5 x 10(-9) and 5 x 10(-8) mol neostigmine demonstrated an effect similar to that of 1 x 10(-9) mol neostigmine. Epinephrine was shown to be the only agent involved in the hyperglycemic response to intraventricular bombesin at doses of 1 x 10(-10), 1 x 10(-9), and 1 x 10(-8) mol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relative contribution of nervous system and hormones to CNS-mediated hyperglycemia is determined by the neurochemical specificity in the brain. 180 63

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.
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PMID:Temporal relations of the endocrine response to exercise. 187 87

To investigate the effects of 14 days administration of H2-receptor antagonist (famotidine) on gastric gastrin and somatostatin secretion, bombesin and glucagon were perfused in the isolated pancreas-duodenum deprived rat stomach. Then serum gastrin concentration, gastric mucosal gastrin and somatostatin content, and gastric mucosal G-cell and D-cell numbers were examined. The 14 days administration of famotidine caused the significant increase of basal gastrin secretion, antral G-cell hyperplasia, high gastrin sensitivity to the stimulation by bombesin, and the low somatostatin sensitivity to the stimulation by glucagon. These facts would suggest that 14 days famotidine administration disturbed not only gastrin secretion but also somatostatin secretion. These results may contribute, at least in part, to the high recurrence of ulcers after withdrawal of H2-receptor antagonists.
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PMID:[Effects of H2-receptor antagonist on gastrin and somatostatin secretion of rat stomach]. 198 91

Bombesin has been shown to decrease food intake and increase the duration of slow wave sleep, as well as to increase blood glucose and glucagon. A suspected mechanism of bombesin's anorexigenic and hypnogenic action could be via its possible effect on the enhancement of metabolism itself. Therefore, the effect of bombesin on rat metabolism was investigated in an open circuit computerized respirometer. This device was specifically conceived to extract the fraction of metabolism which is not due to the energy cost of muscular effort. This fraction of metabolism was designed background metabolism. In the absence of food, peripheral administration of bombesin increased the background metabolism at all doses. The higher dose of bombesin (32 micrograms/kg IP) elicited a four-hour enhancement of background metabolism, the magnitude of which was equivalent to that induced by a meal of about 1.5 grams. Therefore, it is suggested that the effect of bombesin on feeding and sleep could be achieved, at least partly, by its effect on the background metabolism, which ultimately may modulate the behavioral responses.
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PMID:Peripheral administration of bombesin increases metabolism in the rat. 206 20


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