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)

Increased gastric acid secretion occurs after extensive intestinal resection in man, dog, rat, and monkey. Hypergastrinemia has been observed in patients with short gut syndrome and appears to accompany the hyperacidity after intestinal resection in dog, rat, and monkey. Postresectional hypergastrinemia is caused by increased release of gastrin and/or decreased degradation of the hormone. Other hormonal changes after extensive resection include increased insulin, GIP, pancreatic glucagon, and decreased enteroglucagon.
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PMID:Hyperacidity and hypergastrinemia following extensive intestinal resection. 11 43

Gastrin is released by food rich in proteins and by vagal mechanisms. HCI and possibly secretin and glucagon inhibit gastrin release. In the wide range of actions of gastrin, stimulation of gastric acid secretion is the most important. With the advent of radioimmunochemical methods for the determination of gastrinaemia, it has been shown that gastrin exists in a number of forms of different molecular weight. To estimate the validity of gastrin radioimmunoassay it is necessary to demonstrate that decrease in antibody-bound labelled antigen is unrelated to non-specific interference by unknown substances present in serum samples, and that the antiserum reacts with endogenous hormone in an identical manner. Heterogeneity of gastrin in serum may affect the validity of the radioimmunoassay. Hypergastrinaemia associated with hyper-normochlorhydria occures in gastrinoma, hyperplasia of antral gastrin cells, diseases with delayed gastric emptying, retained antrum, short bowel syndrome,renal failure. Hypergastrinaemia associated with hypo-achlorhydria occurs in atrophic gastritis without extensive antral lesion and after vagotomy. Gastrin radioimmunoassay can be used for the mass screening of subjects with atrophic gastritis, a high risk group for gastric cancer.
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PMID:[Gastrin]. 123 74

The present study was designed to examine the role of electrode position during retrograde pacing in dogs with short bowel syndrome and unsevered intact duodenum. In nine beagle dogs a subtotal resection of the small bowel and jejunoileostomy was performed. In five of these dogs, an isolated blind loop (jejunum) with preserved mesenteric connections was left in situ as an additional place for a stimulation electrode. Small intestinal motility and plasma levels of insulin, glucagon, gastrin, somatostatin, and glucose were examined during pacing of the residual jejunum or the isolated loop, respectively, compared with control experiments in the same dogs without pacing. During pacing of the loop a significant (P less than 0.05-0.01) decrease in the postprandial small intestinal motility index was observed combined with a significant (P less than 0.05) increase in plasma insulin levels, whereas the postprandial increase in glucagon, somatostatin, gastrin, and glucose levels was not different from that in controls. In contrast, pacing of the jejunum increased postprandial small intestinal motility index (less than or equal to 68%), whereas the levels of the four hormones and plasma glucose were not different from those in controls. The data suggest that in dogs with intact duodenum, pacing on an excluded loop is required to obtain the desired effect of reduced intestinal motility and improved anabolic pancreatic hormone secretion.
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PMID:Effect of enteric pacing on intestinal motility and hormone secretion in dogs with short bowel. 167 85

To evaluate whether the small bowel can be distracted by mechanical stress in analogy to limb lengthening by osteodistraction, a gut-lengthening apparatus was designed. This distractor was placed at the antimesenterical side of a defined jejunum segment in rabbits. Distraction was performed by 1 mm lengthening of the distractor once daily using extracorporal screws. An effective gut lengthening was achieved of 9.9 +/- 0.5 mm (approximately 100%) within 3 weeks. Treated animals gained weight and remained in good general condition. Fasting plasma levels of cholecystokinin, neurotensin, glucagon-like peptide-1, gastric inhibitory polypeptide, and insulin remained unaffected. Postoperative factor XIII levels were significantly diminished and gastrin was elevated during gut distraction. DNA and protein concentrations in the mucosa of the distracted gut segments corresponded to controls. Mucosal lactase and saccharase activities were reduced. In the distracted bowel segments total tunica muscularis thickness was more than doubled due to muscle cell hypertrophy. In distracted segments villous width was increased. Detection of proliferating mucosal crypt cells utilizing BrdUrd labeling revealed no effects. In conclusion, small gut lengthening by mechanical distraction is possible without major changes in gut morphology. This technique may hint a novel experimental approach for the treatment of short bowel syndrome.
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PMID:Small bowel lengthening by mechanical distraction. 924 19

Factors that stimulate gut mucosal proliferation may be beneficial during periods of gut disuse or atrophy. Recently glucagon-like peptide 2 (GLP-2) has been shown to stimulate small bowel growth. The purpose of our study was to compare the trophic effects of GLP-2 with those of neurotensin (NT), a potent gut trophic factor. Mice were randomized to receive either GLP-2, NT, or saline solution (control) for 10 days. The mice were killed on day 11, at which time the jejunum, ileum, and colon were removed, weighed, and DNA and protein content measured. Mice treated with GLP-2 showed a significant increase in the weight of the jejunum, ileum, and colon compared to both control and NT-treated mice. DNA content, a marker of cellular hyperplasia, was significantly increased in the small bowel and colon by treatment with GLP-2 and NT compared to control tissues. Small intestinal protein content, an indicator of cellular hypertrophy, was significantly increased by GLP-2 compared to both NT and control; protein content of the colon was greater in each of the treatment groups compared with control mice. We have demonstrated, for the first time, that GLP-2 stimulates colonic growth. In addition, GLP-2 is a potent trophic factor of normal small intestine with proliferative effects that are equal to or greater than those of NT. Administration of GLP-2 may be useful clinically to enhance small intestinal regeneration and adaptation during periods of disease and in the early phases of the short bowel syndrome.
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PMID:Glucagon-like peptide 2 is a potent growth factor for small intestine and colon. 983 10

Recent successful synthesis of human glicentin prompted us to establish an immunoassay method for determination of human glicentin in plasma. Human glicentin in plasma was measured using a newly developed sandwich ELISA. The mean fasting levels of human glicentin were 18.6+/-2.4 and 19.7+/-2.1 pM in normal subjects and diabetic patients, respectively. In diabetic patients with renal failure, plasma glicentin was elevated, exceeding 100 pM. In normal subjects, plasma glicentin increased to a peak level of about 130 pM at 60 min after an oral glucose load, and then decreased. In patients who underwent gastrectomy, plasma glicentin rapidly increased to a peak of about 300 pM at 30 min after oral glucose load. In a patient with short bowel syndrome plasma glicentin did not change following an oral glucose load. These results correspond with previous findings for gut glucagon-like immunoreactive materials (GLI) or enteroglucagon. We conclude that glicentin is secreted from the small intestine in response to intraluminal glucose stimulation in humans.
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PMID:Plasma glicentin in diabetic and gastrectomized patients. 993 May 83

Glucagon-like peptide 2 (GLP-2) is secreted in a nutrient-dependent manner from enteroendocrine cells throughout the gastrointestinal tract and is trophic to the intestinal epithelial mucosa. GLP-2 acts via stimulation of crypt cell proliferation and inhibition of cell death. GLP-2 also stimulates intestinal glucose transport, decreases mucosal permeability, and shows therapeutic efficacy in experimental models of short bowel syndrome and both small and large bowel inflammation.
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PMID:Glucagon-like Peptide 2. 1032 10

Combination therapy with enterotrophic agents may be useful in patients with the short bowel syndrome. The gut hormones neurotensin (NT) and glucagon-like peptide 2 (GLP-2) are potent enterotrophic factors when administered alone; however, their combined effects are not known. Using a GLP-2-producing tumor (STC-1), we determined whether administration of NT enhances the effect of GLP-2 on intestinal growth. Athymic mice were injected with STC-1 cells (6 x 10(6)) subcutaneously. Twenty-three days after STC-1 implantation, mice received either NT (300 microg/kg or 600 microg/kg) or saline solution (control) subcutaneously three times a day for 6 days. Two groups of tumor-free mice received either saline or NT for 6 days. At sacrifice, jejunum and ileum were collected, weighed, and analyzed for DNA and protein content. In the jejunum, NT combined with GLP-2 (from STC-1) increased weight, protein content (markers of mucosal hypertrophy), and DNA content (a marker of mucosal hyperplasia), compared to either NT or GLP-2 alone. In the ileum, the combination of NT and GLP-2 significantly increased weight and/or protein content compared to NT or GLP-2 alone. Administration of NT enhances the enterotrophic effects of GLP-2, augmenting hypertrophy of the entire small bowel and hyperplasia of the jejunum. The combination of NT and GLP-2 may be useful to enhance intestinal growth in patients with the short bowel syndrome.
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PMID:Enterotrophic effects of glucagon-like peptide 2 are enhanced by neurotensin. 1048 97

Several lines of evidence demonstrate that general nutritional status, specific nutrients (eg, zinc, glutamine), and certain trophic growth factors (eg, growth hormone, insulin-like growth factor I, keratinocyte growth factor, and glucagon-like peptide-2) have important interactions relevant for intestinal growth and function. Adequate nutritional status is critical for endogenous growth factor synthesis in the gut and other tissues and is an important mediator of organ responsiveness to exogenous growth factor administration. Both endogenously synthesized and exogenously administered growth factors upregulate nutrient uptake and utilization by gut mucosa, skeletal muscle, and other organs. Emerging data from both animal and human studies indicate that combinations of selected growth factors and specific nutrients may improve the growth, adaptation, and repair of the intestinal mucosa. Additional studies to determine basic mechanisms of nutrient-growth factor interactions and the safety and efficacy of treatment with combinations of specific nutrients and recombinant growth factors are needed. Results of these investigations should define new methods for support of the intestinal tract during short bowel syndrome (SBS), catabolic illness, and malnutrition.
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PMID:Interactions between nutrients and peptide growth factors in intestinal growth, repair, and function. 1057 52

Glucagon-like peptide 2 (GLP-2) is a 33 amino acid peptide-encoded carboxyterminal to the sequence of GLP-1 in the proglucagon gene. Both GLP-1 and GLP-2 are secreted from gut endocrine cells and promote nutrient absorption through distinct mechanisms of action. GLP-2 regulates gastric motility, gastric acid secretion, intestinal hexose transport, and increases the barrier function of the gut epithelium. GLP-2 significantly enhances the surface area of the mucosal epithelium via stimulation of crypt cell proliferation and inhibition of apoptosis in the enterocyte and crypt compartments. The cytoprotective and reparative effects of GLP-2 are evident in rodent models of experimental intestinal injury. GLP-2 reduces mortality and decreases mucosal injury, cytokine expression, and bacterial septicemia in the setting of small and large bowel inflammation. GLP-2 also enhances nutrient absorption and gut adaptation in rodents or humans with short bowel syndrome. The actions of GLP-2 are transduced by the GLP-2 receptor, a G protein-coupled receptor expressed in gut endocrine cells of the stomach, small bowel, and colon. Activation of GLP-2 receptor signaling in heterologous cells promotes resistance to apoptotic injury in vitro. The cytoprotective, reparative, and energy-retentive properties of GLP-2 suggests that GLP-2 may potentially be useful for the treatment of human disorders characterized by injury and/or dysfunction of the intestinal mucosal epithelium.
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PMID:Glucagon-like peptide 2. 1129 14


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