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)

Endogenous opioid peptides appear to play a role in the initiation of feeding. Butorphanol, an exogenous opiate which preferentially generalizes to the kappa-sigma opiate receptors, is a potent initiator of feeding. In these studies, we examined the effect of peripherally administered putative satiety substances, cholecystokininoctapeptide, somatostatin, bombesin, gastrin-releasing peptide, thyrotropin-releasing hormone, calcitonin and glucagon on butorphanol induced feeding. With the exception of bombesin, all the other putative satiety factors required 2 to 32 times as high a dose to significantly suppress feeding following butorphanol compared to the dosages required to suppress starvation or tail pinch induced feeding. Bombesin appeared to be approximately equipotent in all systems tested. Haloperidol and atropine both suppressed butorphanol induced feeding supporting our previous hypothesis of an integral relationship between acetylcholinergic-dopaminergic and opioid mechanisms in the initiation of feeding. The findings reported here are compatible with an important role for opioid mechanisms in the initiation of feeding.
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PMID:The effect of peripherally administered satiety substances on feeding induced by butorphanol tartrate. 631 70

The influence of iv administration of 0.2 mg thyrotropin-releasing hormone (TRH) on serum calcium was examined in 20 subjects divided into three different groups: one, comprising patients with primary hypothyroidism (A), another, containing euthyroid patients with various diseases (B), and a third, including healthy volunteers (C). Ninety min after the TRH injection total serum calcium (T-Ca) had fallen by 0.19 +/- 0.03 mmol/l in group A (p less than 0.01), by 0.10 +/- 0.02 mmol/l in group B (p less than 0.01), and by 0.08 +/- 0.02 mmol/l in group C (p less than 0.02). Ionized serum calcium (I-Ca) fell in parallel with T-Ca in group A and B. In contrast, serum magnesium was unaffected in all groups. Neither the renal excretion of calcium nor the serum concentration of parathyroid hormone, glucagon or calcitonin changed significantly in response to TRH. These results indicate that TRH has a slight hypocalcemic effect in man which is not caused by plasma dilution, direct influence on the kidneys, or TRH effects on the major calcium regulating hormones. Whether TRH per se, or an increased serum TSH level, induces calcium to leave the vascular space remains to be elucidated.
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PMID:Serum calcium decline after intravenous administration of thyrotropin-releasing hormone in man. 640 74

The hypothalamus is known to participate in the control of carbohydrate and lipid metabolism and, therefore, the hypothalamic thyrotropin-releasing hormone, TRH, could possibly be involved in these control functions. Moreover, TRH immunological and biological activities have been demonstrated in the pancreatic islets, but experiments with isolated rat pancreas have failed to show any direct stimulatory effect of TRH on glucagon and insulin release. In order to study any in vivo effects of TRH on the pancreatic hormone release and the plasma levels of glucose and free fatty acids, TRH was injected intravenously into fasted rabbits, and blood samples obtained from the marginal ear vein. Dose-related increases in plasma levels were observed for glucagon, insulin, glucose and free fatty acids down to a dose of 0.4 microgram TRH. Corresponding experiments showed that the tripeptide pyroGlu-His-GlyOH was inactive. The increase of plasma levels of glucagon was augmented by simultaneous injection of TRH and insulin, and was suppressed in rabbits which were fed or infused with somatostatin. This suggests that TRH may have physiological significance in modulating the plasma levels of glucagon, insulin, glucose and free fatty acids. In contrast to the effect of alanine, the increase in plasma levels of glucagon by TRH was not significant during the first 10 minutes. This suggests that the effect to TRH on glucagon and insulin release is indirect.
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PMID:Thyrotropin-releasing hormone increases plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits. 679 23

Mild tail pinch (TP) in rats resulted in 72% of animals displaying ingestive behavior with 20% demonstrating gnawing behavior without food ingestion and 8% demonstrating licking behavior only. The animals ate steadily over 5 min with a maximum rate occurring at 1 min (0.5 +/- 0.2 g). There was a circadian rhythm of TP-induced behavior with the peak food ingestion occurring at 24 h. A mild increase in blood glucose occurred 120 s after commencement of TP (115 +/- 4 mg/dl). Common satiety signals such as stomach distension and glucose decreased food ingestion. Parenteral administration of glucagon, cholecystokinin-octapeptide, bombesin, and thyrotropin-releasing hormone resulted in suppression of TP-induced food ingestion. Chronic TP (12 5-min TP periods/day) resulted in a fall in spontaneous food intake with the total intake remaining similar to food intake prior to the chronic TP period. We suggest that TP serves as an excellent model for eating behavior because 1) it correlates well with starvation-induced eating; 2) it precludes the necessary deprivation of food and water to adrenalectomized animals; and 3) animals subjected to TP continue chewing in the face of decreased food intake allowing one to exclude the possibility that the effects of an anorectic are secondary to nausea.
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PMID:Stress-induced eating in rats. 719 55

Interleukin-1, tumor necrosis factor, and interleukin-6 inhibit insulin release and may be cytotoxic to isolated pancreatic islets. These cytokines have been postulated to play an important role in the beta cell destruction characteristic of type 1 diabetes. The present study was designed to investigate the effect of the above cytokines on insulin, glucagon, somatostatin, and thyrotropin-releasing hormone secretion by isolated human islets. In addition, we have investigated if cytokine-induced modifications in hormone secretion are accompanied by modifications in the ab initio synthesis of any specific lipidic fraction. All three cytokines studied, although not modifying insulin and somatostatin release to glucose 5 mmol/L, inhibited the response of both hormones to glucose 20 mmol/L. On the other hand, the cytokines almost completely blocked islet basal glucagon release, without affecting thyrotropin-releasing hormone secretion. The added cytokines also suppressed 20 mmol/L [U-14C]glucose incorporation into both phospholipids and diacylglycerol. Our results demonstrate a beta-, alpha-, and delta-cell, sensitivity to cytokine action. Additionally, they suggest that ab initio lipid synthesis might be implicated in the mechanism of insulin release in human islets.
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PMID:Cytokine-induced inhibition of lipid synthesis and hormone secretion by isolated human islets. 802 53

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-MSH increase food intake whereas insulin, glucagon, cholecystokinin, anorectin, corticotropin releasing hormone, neurotensin, bombesin, enterostatin, cyclo-his-pro and thyrotropin-releasing hormone reduce food intake. A number of these peptides also affect the activity of the sympathetic nervous system. The peptides which have been tested have a reciprocal effect on food intake and sympathetic activity. Opioids, NPY and GHRH, which increase food intake, decrease sympathetic activity. Conversely, peptides which reduce food intake, increase sympathetic activity, with glucagon, cholecystokinin, corticotropin releasing hormone, calcitonin, neurotensin and bombesin being examples, Several of these peptides also affect the intake of specific nutrients. Insulin reduces food intake in animals fed a high carbohydrate diet, but not when fed a high fat diet. Neuropeptide Y increases carbohydrate intake. Galanin and opioid peptides increase fat intake. Enterostatin and cyclo-His-Pro, on the other hand reduce fat intake. Glucagon decreases protein intake. The effect of peptides on the intake of 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:The nutrient balance hypothesis: peptides, sympathetic activity, and food intake. 848 34

Reports of characteristic psychiatric symptoms occurring in patients with pancreatic cancer appear regularly in the literature. A review of this literature reveals that symptoms of depression and/or anxiety may appear in approximately 50% of patients with pancreatic cancer before the diagnosis is made. This review proposes that the psychopathology of pancreatic tumors may be linked to tumor-induced changes in neuroendocrine or acid-base systems. Although confirmatory data are lacking, informed speculation centers on the potential role of adrenocorticotropic hormone, parathyroid hormone, thyrotropin-releasing hormone, glucagon, serotonin, insulin, and bicarbonate in the production of depression and/or anxiety in this disease. Elucidation of the pathophysiology of the psychiatric symptoms in patients with pancreatic cancer may provide a marker for early diagnosis of pancreatic neoplasia as well as a probe into the biologic bases of depression and anxiety.
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PMID:Psychopathology of pancreatic cancer. A psychobiologic probe. 849 2

Many peptides have been shown to modulate nutrient intake. In most cases, these peptides decrease food intake, but in a few cases they have been demonstrated to stimulate feeding. Infusion of insulin peripherally will decrease food intake unless hypoglycemia occurs where the reduced glucose is a stimulus to feeding. Other pancreatic hormones including glucagon, amylin, pancreatic polypeptide, and enterostatin reduce food intake. Of the gastrointestinal hormones, cholecystokinin has been the most widely studied and reduces food intake in a number of species, including human beings. Gastrin-releasing peptide and its relative bombesin have been shown to decrease food intake in experimental animals and man. Somatostatin reduces food intake in experimental animals, but no clinical studies are available. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte stimulating hormone (dMSH), growth hormone, and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides which modulate feeding. beta-casomorphin, a hepta peptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines, and thyrotropin-releasing hormone decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors which relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.
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PMID:Nutrient intake is modulated by peripheral peptide administration. 869 60

Tumor necrosis factor (TNF alpha) has been shown to inhibit insulin release and it has been postulated to-be an important effector in islet rejection. We studied the effect of cryopreservation on glucose oxidation rate (GOR), lipid synthesis, hormone secretion (insulin, glucagon, somatostatin, thyrotropin-releasing hormone), and cyclic guanosine 3',5'-monophosphate (cGMP) content of human islets, in the presence or absence of TNF alpha, looking for changes that could explain a different susceptibility to rejection for cryopreserved islets. Islets were isolated from multiple organ donor pancreata by collagenase digestion. The islets were then cultured for 7 days, cryopreserved (-0.25 degrees C/min), and stored in liquid N2. After 24 h of culture, thawed islets were cultured for an other 24 h in the presence or absence of TNF alpha. Islets were then washed to remove the cytokine and incubated in Krebs-Ringer bicarbonate (5 or 20 mM glucose), and both the cGMP content of the islets and the hormone concentration in the medium were determined by radio-immunoassay. GOR was measured as the production of 14CO2 from 5 or 20 mM D-[U-14C]glucose, and de novo lipid synthesis was determined as D-[U-14C]glucose incorporation into different lipidic fractions. Cryopreservation did not significantly modify the hormone response to glucose but it partially reversed the TNF alpha-induced inhibitory effect on insulin release in the presence of 20 mM glucose. In addition, the inhibitory effect of TNF alpha on phosphatidylcholine labeling was attenuated in cryopreserved islets compared with noncryopreserved islets. TNF alpha significantly stimulated islet nitrite production and cGMP accumulation, both effects being of a similar magnitude in cryopreserved and noncryopreserved islets. Our results suggest that cryopreservation can modify the metabolic and hormone response of human islets to TNF alpha. This effect is not mediated by changes in the TNF alpha-induced islet nitric oxide production or cGMP accumulation.
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PMID:Influence of cryopreservation on the sensitivity of human islets to tumor necrosis factor. 878 31

The dorsal vagal complex (DVC) and nucleus raphe obscurus (nROb) are currently known to control vagal outflow to the stomach and the pancreas. Elucidation of neurotransmitters in these nuclei that control vagal outflow has become necessary to determine the endogenous circuitry for control of gastric motor activity and pancreatic hormone secretion. In this review, the author's data on the effects of selected peptides on intragastric pressure and gastric contractility as well as on pancreatic glucagon and insulin secretion in the DVC and nROb are presented. Microinjection of thyrotropin-releasing hormone (TRH) or pituitary adenylate cyclase-activating polypeptide (PACAP38) into the nROb results in gastric excitatory motor responses, whereas substance P (SP) and vasoactive intestinal polypeptide (VIP) evoke gastric relaxation. Irrespective of colocalization of TRH and SP in the serotonergic neurons of the nROb, these peptides independently affect gastric motor function when microinjected into the nROb. The inhibitory effect of SP on gastric motor function in the nROb is apparently mediated via nitric oxide in the DVC and involves peripheral VIP, acetylcholine, gamma-aminobutyric acid and nitric oxide. Microinjection of endothelin, PACAP38, and VIP into the DVC evokes increases in gastric motor activity. Pancreatic polypeptide, microinjected into the DVC, does not affect basal plasma insulin and glucagon concentration but potentiates glucose-stimulated insulin secretion. All these data make an important contribution to our understanding of the vagal mechanisms controlling gastric motor and endocrine pancreatic function.
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PMID:Role of selected peptides in the vagal regulation of gastric motor and endocrine pancreatic function. 887 96


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