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)

Quantitative changes in the glycogen granula contents of the dog's small intestinal mucosa were investigated with light microscopy using Best-carmin dying. In fasting animals the glycogen could be detected in a patchy arrangement in the supranuclear cytoplasmic region of the enterocytes. During glucose abasorption glycogen appeared in continually increasing quantities also in the lamina propria. Injecting Glucagon (50-100 microgram/15') into the artery of the intestinal loop during glucose absorption, glycogen totally disappeared from the enterocytes, while it remained unchanged in the cells of the lamina propria.
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PMID:[Changes in the structural localization of glycogen during glucose resorption]. 90 4

Clinical evidence is presented supporting the hypothesis that the metabolic abnormality in the dystrophin-defective muscular dystrophies (DMD and BMD) involves the ATP pathway. Objective laboratory data show corrective trends in the abnormal values of parameters relating to creatine and calcium metabolism (ATP) by use of glucagon-stimulated c-AMP and by use of synthetically produced adenylosuccinic acid (ASA). Disease accelerating mechanisms as suggested by analysis of the clinical features, and the therapeutic potential of ASA are discussed.
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PMID:The dystrophin connection--ATP? 132 12

In the islets of the rat pancreas, steroid diabetes induced by triamcinolon-acetonid leads to degranulation of the B cells and glycogen infiltration. The glycogen cannot be satisfactorily detected using methods like the chromic acid technique according to Bauer, staining with Best's carmine, or the usually applied periodic acid-Schiff (PAS) reaction. Glycogen detection is improved, however, when lead tetraacetate is used in place of periodic acid as oxidizing agent. When combining the carbohydrate detection method with the peroxidase--antiperoxidase (PAP) method used for immunocytochemical detection of the various pancreatic islet hormones, paraffin sections reveal that glycogen is primarily localized in granulated B cells; the degranulated B cells also contain glycogen, though in smaller amounts. In contrast, the islet cells containing somatostatin, glucagon and pancreatic polypeptide are nearly free of glycogen.
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PMID:Glycogen in pancreatic islets of steroid diabetic rats. Carbohydrate histochemical detection and localization using an immunocytochemical technique. 703 7

Patients with beta-thalassemia major (beta-thalassemia) frequently have bone disorders of multifactorial etiology. We attempted to analyze the relationship between the bone mineral density ([BMD] measured by dual-photon absorptiometry) and auxanologic parameters, degree of siderosis, function of the growth hormone (GH)/insulin-like growth factor-I (IGF-I)/IGF-binding protein-3 (IGFBP3) axis, calcium-phosphate balance, parathyroid hormone (PTH), and cytokines (interleukin-1beta [IL-1] and tumor necrosis factor-alpha [TNF-alpha]) in 30 prepubertal children with beta-thalassemia major and 15 age-matched children with constitutional short stature (CSS), who have normal glucose tolerance and thyroid function. Children with beta-thalassemia had a significantly decreased BMD and mean BMD% for age and sex (0.75+/-0.24 g/cm2 and 71%+/-10%, respectively) versus children with CSS (1.06+/-0.3 g/cm2 and 92%+/-7%, respectively). Thalassemic patients had significantly lower circulating concentrations of IGF-I and IGFBP3 (49+/-21 ng/mL and 1.2+/-0.25 mg/L, respectively) compared with control children (153+/-42 ng/mL and 2.1+/-0.37 mg/L, respectively). The GH response to provocation by clonidine and glucagon was defective (peak GH < 7 microg/L) in 12 of the 30 thalassemic children. Serum concentrations of IL-1beta and TNF-alpha did not differ among the two study groups. Hypocalcemia was detected in five of the 30 thalassemic patients: hypoparathyroidism was diagnosed in two of the five and rickets in the other three. BMD was highly correlated with the circulating concentrations of IGF-I and IGFBP3, as well as with the auxanologic parameters (age, weight, height, height standard deviation score [HSDS], and body mass index [BMI]). It is suggested that increasing the circulating IGF-I concentration through aggressive nutritional therapy and/or GH/IGF-I therapy with supplementation with vitamin D and/or calcium might improve bone growth and mineralization and prevent the development of osteoporosis and consequent fractures in these patients. Such therapy requires blinded controlled trials.
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PMID:Bone mineral density in prepubertal children with beta-thalassemia: correlation with growth and hormonal data. 959 44

The purpose of this chapter is to examine the possible role of platelet-activating factor (PAF) antagonist therapy as a means of modifying the systemic inflammatory response syndrome (SIRS) and multi-organ dysfunction syndrome (MODS) in the management of patients with severe acute pancreatitis (AP). Supposed specific treatments of AP have not shown clinical benefit, with antiprotease agents such as aprotinin and gabexate mesilate, as well as fresh frozen plasma, being ineffective. In addition, early peritoneal lavage, intravenous glucagon, somatostatin and octreotide have shown no benefit.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:The possible role of platelet-activating factor antagonist therapy in the management of severe acute pancreatitis. 1103 Jun 12

Patients who suffer from intestinal failure depend on parenteral support to maintain nutritional equilibrium. In this chapter, recommendations for evaluation the absorptive capacity of patients with intestinal failure are defined, and the evidence and magnitude of the effect of dietary and hormone therapy is given. Regarding dietary advice, the effects of employment of diets with various carbohydrate:fat ratios in short-bowel syndrome (SBS) patients with and without a preserved colon is presented. Focus has been placed on the use of growth hormone but also on the use of a novel intestinotrophic hormone, glucagon-like peptide 2, in the promotion of intestinal adaptation in SBS patients. Overall, the ultimate aim in the treatment of SBS patients is to optimize remnant intestinal function, thereby eliminating the need for parenteral support and improving quality of life in these patients.
Best Pract Res Clin Gastroenterol 2003 Dec
PMID:Experimental approaches: dietary and hormone therapy. 1464 64

The glucagon-like peptides (glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2)) are released from enteroendocrine cells in response to nutrient ingestion. GLP-1 enhances glucose-stimulated insulin secretion and inhibits glucagon secretion, gastric emptying and feeding. GLP-1 also has proliferative, neogenic and antiapoptotic effects on pancreatic beta-cells. More recent studies illustrate a potential protective role for GLP-1 in the cardiovascular and central nervous systems. GLP-2 is an intestinal trophic peptide that stimulates cell proliferation and inhibits apoptosis in the intestinal crypt compartment. GLP-2 also regulates intestinal glucose transport, food intake and gastric acid secretion and emptying, and improves intestinal barrier function. Thus, GLP-1 and GLP-2 exhibit a diverse array of metabolic, proliferative and cytoprotective actions with important clinical implications for the treatment of diabetes and gastrointestinal disease, respectively. This review will highlight our current understanding of the biology of GLP-1 and GLP-2, with an emphasis on both well-characterized and more novel therapeutic applications of these peptides.
Best Pract Res Clin Endocrinol Metab 2004 Dec
PMID:Clinical endocrinology and metabolism. Glucagon-like peptide-1 and glucagon-like peptide-2. 1553 74

The 42 amino acid polypeptide glucose-dependent insulinotropic polypeptide/gastric inhibitory polypeptide (GIP) is released from intestinal K-cells in response to nutrient ingestion. Based on animal studies, the peptide was initially assumed to act as an endogenous inhibitor of gastric acid secretion. Later it was found that GIP is capable of augmenting glucose-stimulated insulin secretion, and subsequent studies provided evidence that, in humans, the peptide predominantly acts as an incretin hormone. A role for GIP in the regulation of lipid homeostasis and in the development of obesity has been inferred from different animal studies. While GIP strongly stimulates insulin release in healthy humans, the peptide has almost completely lost its insulinotropic effect in patients with type 2 diabetes. This is different from the actions of glucagon-like peptide 1, which stimulates insulin secretion even in the later stages of type 2 diabetes. This suggests that a diminished insulinotropic effect of GIP may contribute to the pathogenesis of type 2 diabetes. This review will summarize the actions of GIP in human physiology and discuss its role in the pathogenesis of type 2 diabetes, as well as the therapeutic options derived from these findings.
Best Pract Res Clin Endocrinol Metab 2004 Dec
PMID:Clinical endocrinology and metabolism. Glucose-dependent insulinotropic polypeptide/gastric inhibitory polypeptide. 1553 77

The gastric emptying rate is a carefully regulated process consisting of different mathematically defined phases. The gastric metabolic load, as well as neural regulatory mechanisms and hormonal influences, cooperate in order to achieve a well-balanced emptying of contents from the stomach into the duodenum for absorption in the small intestine. This finely tuned regulation is primarily regulated by the release of gastrointestinal peptide hormones which serve to counteract the emptying process in the fed state and to stimulate sweeping contractions in the fasted state, most likely in order to prepare the stomach for another meal. We have found that the two peptide hormones ghrelin and glucagon-like peptide- I (GLP- I) have a great impact on the regulation of gastric emptying: ghrelin is a most potent stimulator of gastric contractions and emptying, and GLP- I profoundly inhibits this emptying process. These data suggest possibilities for governing the rate of gastric emptying as a natural step in achieving metabolic balance and control.
Best Pract Res Clin Anaesthesiol 2006 Sep
PMID:The physiology of gastric emptying. 1708 Jun 92

Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract. Among the specific tumour markers are serotonin and its metabolites--e.g. 5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma. Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma. Among the tumour-non-specific markers are: chromogranins, neuron-specific enolase (NSE), alpha-subunits of the glycoprotein hormones, catecholamines, pancreatic polypeptide (PP), ghrelin and adrenomedullin.
Best Pract Res Clin Endocrinol Metab 2007 Mar
PMID:Biochemistry of neuroendocrine tumours. 1738 64


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