Relevant bibliographies by topics / Glucagon-like peptide 1

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Glucagon-like peptide 1'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "Glucagon-like peptide 1"

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Baggio, Laurie L., and Daniel J. Drucker. "Glucagon-like peptide-1 and glucagon-like peptide-2." Best Practice & Research Clinical Endocrinology & Metabolism 18, no. 4 (December 2004): 531–54. http://dx.doi.org/10.1016/j.beem.2004.08.001.

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Kim, Sung-Gun, and Jong-Tae Park. "Recombinant production of human glucagon-like peptide-1 mutant." Korean Journal of Agricultural Science 41, no. 3 (September 30, 2014): 237–43. http://dx.doi.org/10.7744/cnujas.2014.41.3.237.

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&NA;. "Glucagon-like peptide-1." Inpharma Weekly &NA;, no. 841 (June 1992): 16. http://dx.doi.org/10.2165/00128413-199208410-00022.

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Giblett, Joel P., Sophie J. Clarke, David P. Dutka, and Stephen P. Hoole. "Glucagon-Like Peptide-1." JACC: Basic to Translational Science 1, no. 4 (June 2016): 267–76. http://dx.doi.org/10.1016/j.jacbts.2016.03.011.

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Doyle, M. E. "Glucagon-Like Peptide-1." Recent Progress in Hormone Research 56, no. 1 (January 1, 2001): 377–400. http://dx.doi.org/10.1210/rp.56.1.377.

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Rowzee, Anne M., Niamh X. Cawley, John A. Chiorini, and Giovanni Di Pasquale. "Glucagon-Like Peptide-1 Gene Therapy." Experimental Diabetes Research 2011 (2011): 1–5. http://dx.doi.org/10.1155/2011/601047.

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Glucagon-like peptide 1 (GLP-1) is a small peptide component of the prohormone, proglucagon, that is produced in the gut. Exendin-4, a GLP-1 receptor agonist originally isolated from the saliva ofH. suspectumor Gila monster, is a peptide that shares sequence and functional homology with GLP-1. Both peptides have been demonstrated to stimulate insulin secretion, inhibit glucagon secretion, promote satiety and slow gastric emptying. As such, GLP-1 and Exendin-4 have become attractive pharmaceutical targets as an adjunctive therapy for individuals with type II diabetes mellitus, with several products currently available clinically. Herein we summarize the cell biology leading to GLP-1 production and secretion from intestinal L-cells and the endocrine functions of this peptide and Exendin-4 in humans. Additionally, gene therapeutic applications of GLP-1 and Exendin-4 are discussed with a focus on recent work using the salivary gland as a gene therapy target organ for the treatment of diabetes mellitus.
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Lutz, Thomas A., and Elena Osto. "Glucagon-like peptide-1, glucagon-like peptide-2, and lipid metabolism." Current Opinion in Lipidology 27, no. 3 (June 2016): 257–63. http://dx.doi.org/10.1097/mol.0000000000000293.

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Wang, XingChun, Huan Liu, Jiaqi Chen, Yan Li, and Shen Qu. "Multiple Factors Related to the Secretion of Glucagon-Like Peptide-1." International Journal of Endocrinology 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/651757.

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The glucagon-like peptide-1 is secreted by intestinal L cells in response to nutrient ingestion. It regulates the secretion and sensitivity of insulin while suppressing glucagon secretion and decreasing postprandial glucose levels. It also improves beta-cell proliferation and prevents beta-cell apoptosis induced by cytotoxic agents. Additionally, glucagon-like peptide-1 delays gastric emptying and suppresses appetite. The impaired secretion of glucagon-like peptide-1 has negative influence on diabetes, hyperlipidemia, and insulin resistance related diseases. Thus, glucagon-like peptide-1-based therapies (glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors) are now well accepted in the management of type 2 diabetes. The levels of glucagon-like peptide-1 are influenced by multiple factors including a variety of nutrients. The component of a meal acts as potent stimulants of glucagon-like peptide-1 secretion. The levels of its secretion change with the intake of different nutrients. Some drugs also have influence on GLP-1 secretion. Bariatric surgery may improve metabolism through the action on GLP-1 levels. In recent years, there has been a great interest in developing effective methods to regulate glucagon-like peptide-1 secretion. This review summarizes the literature on glucagon-like peptide-1 and related factors affecting its levels.
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Padwal, R. "Glucagon-like peptide-1 agonists." BMJ 344, jan10 2 (January 10, 2012): d7282. http://dx.doi.org/10.1136/bmj.d7282.

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Müller, T. D., B. Finan, S. R. Bloom, D. D'Alessio, D. J. Drucker, P. R. Flatt, A. Fritsche, et al. "Glucagon-like peptide 1 (GLP-1)." Molecular Metabolism 30 (December 2019): 72–130. http://dx.doi.org/10.1016/j.molmet.2019.09.010.

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Dissertations / Theses on the topic "Glucagon-like peptide 1"

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Armstrong, Matthew James. "Glucagon-like peptide-1 in nonalcoholic steatohepatitis." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/4987/.

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Nonalcoholic fatty liver disease (NAFLD), and in particular its inflammatory component steatohepatitis (NASH), are associated with significant risk of liver/cardiovascular morbidity and death. My findings highlight that NAFLD is now the commonest cause of liver disease in primary care, yet significant numbers with advanced fibrosis remain undetected. Application of simple non-invasive scoring systems could aid with identifying those in greatest need of intervention. By adopting an integrative physiological approach with functional measures of lipid and carbohydrate flux, I demonstrated that patients with NASH (vs. healthy controls) have marked adipose tissue dysfunction (especially in abdominal subcutaneous adipose tissue), alongside increased hepatic and muscle insulin resistance (IR). Targeting adipose-derived lipotoxicity should be the mainstay of therapy in NASH. Glucagon-like peptide-1 (GLP-1) based therapy (liraglutide) appears to be safe and well tolerated in patients at risk of underlying NAFLD. My prospective randomised-controlled study highlighted that liraglutide reduces metabolic dysfunction, hepatic lipogenesis, hepatic/adipose IR and inflammation in patients with NASH. My in vitro studies in human hepatocytes indicate that the anti-steatotic effects are not solely reliant on improvements in weight and/or glycaemic control. Taken together, my findings highlight that GLP-1 based therapies have all the metabolic and clinical attributes to make them a promising therapeutic option in patients with NASH. However, the safety and histological efficacy of such awaits the completion of my 48-week Phase II ‘LEAN’ trial, which is integral as to whether larger clinical trials are warranted.
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Adamczyk, Malgorzata. "The glucoregulatory action of glucagon-like peptide-1 (GLP-1)." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9612.

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Glucagon-like peptide-1 (GLP-1) has been shown to improve tolerance to glucose. It has been suggested that this could be mediated by an incretin effect--the enhancement of insulin secretion in response to glucose, as well as by alterations in the sensitivity of the body to insulin. In order to evaluate the effect of GLP-1 on the improvement of glucose tolerance, the systemic as well as tissue-specific (the liver, intestine and muscle) effects of this hormone have been determined. The study has been conducted on animal model (the pig). Following an overnight fast and baseline measurements, glucose was infused (set point = 150 mg/dl), alone or supplemented with GLP-1 (4 ng/kg/min) and GLP-1 (8 ng/kg/min) in 90 min steps. The levels of metabolites (glucose, lactate) and hormones (insulin, glucagon, GLP-1) were then determined in arterial blood as well as in portal, hepatic and femoral venous blood. Tissue balances were then calculated. Levels of metabolites and hormones, glucose infusion rates and tissue balances were compared using statistical analysis (general linear models procedure, SAS Institute). (Abstract shortened by UMI.)
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Brynes, Audrey. "Dietary intake, glucagon like peptide-1 and insulin sensitivity." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326161.

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Paternoster, Silvano. "Lysophosphatidylinositol-glucagon like peptide 1 crosstalk in metabolic diseases." Thesis, Curtin University, 2020. http://hdl.handle.net/20.500.11937/81689.

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This PhD thesis discusses the study of a novel class of drugs for the treatment of metabolic diseases. We have characterized the pharmacology and biology of the lipid Oleoyl-lysophosphatidylinositol (Oleoyl-LPI), and we show that some synthetic molecules mimicking its structure, are efficient glucagon-like peptide-1 (GLP-1) secreting drugs in vitro and in vivo in diabetic mice. We have also dissected the pharmacology of Cannabis-derived drugs and demonstrated that they can also modulate GLP-1 secretion.
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Khatib, Oussama-Mohmad. "Peripheral and central effect of glucagon-like peptide-1 (GLP-1)." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244094.

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Bose, Amal Krishna. "Glucagon like peptide-1 (GLP-1) in myocardial ischaemia-reperfusion injury." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445399/.

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Glucagon-Like Peptide-1 (GLP-1) is an incretin hormone released by enteroendocrine cells lining the intestine in response to the presence of nutrients. GLP-1 is known to cause increased secretion of insulin from the pancreas and has been identified as one of the crucial components of insulin and in turn glucose homeostasis. GLP-1 has a very short half life of 1-2 minutes, being rapidly degraded by a ubiquitous enzyme called dipeptidyl dipeptidase IV and also undergoing renal excretion. Interestingly GLP-1 mRNA transcripts have been identified in several organs outside of the expected enteropancreatic axis including the heart. Insulin has been shown to reduce cell death in the ischemic-reperfused rat myocardium and in isolated rat myocytes via its ability to activate prosurvival kinase signalling pathways. We propose that GLP-1 could protect the myocardium against ischaemia-reperfusion injury by activating similar prosurvival signalling pathways. Both in-vivo (open chest) and in-vitro (Langendorff perfused) rat heart models of regional ischaemia and reperfusion were used. In-vivo treatment with GLP-1 produced a significant reduction in infarction (% infarct/risk zone) compared to valine pyrrolidide (VP), (an inhibitor of the enzyme dipeptidyl peptidase), and control groups (20.0 2.8, vs. 47.3 4.3, and 44.3 2.4, respectively PO.001). In isolated perfused hearts (where there is no circulating insulin) GLP-1 significantly reduced infarct size compared to VP and control (26.7 2.7 vs. 52.6 4.7 and 58.7 4.1, PO.001) groups respectively. Protection was abolished in the presence of the PI3kinase inhibitor, LY294002 (58.6 4.1), the ERK 1/2 MAPK inhibitor, U0126 (48.3 8.6), the p70s6K inhibitor, Rapamycin (57.1 4.9%) and by the GLP-1 receptor antagonist exendin-9-39 (57.3 3.8). GLP-1 protects the myocardium against ischaemic - reperfusion injury when given throughout ischaemia - reperfusion or when given just five minutes prior to the onset of reperfusion or as a preconditioning mimetic. To further elucidate the mechanism of GLP-1 mediated myocardial preservation we carried out Western blot studies examining the phosphorylation of components of the RISK pathway which showed an increase in the phosphorylation of BAD. The increased phosphorylation of the pro-death peptide BAD, confirmed the potential anti- apoptotic effect of GLP-1. In conclusion we have demonstrated for the first time that GLP-1 protects the rat myocardium against ischaemia-reperfusion injury, both in vivo and in vitro. GLP-1 appears to protect via the up regulation of specific prosurvival kinase pathways. This may represent a new therapeutic potential for this class of drugs currently undergoing trials in the treatment of non-insulin dependent diabetes.
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Sinclair, Elaine M. "GLP-1 effects on pancreatic b-cell lines." Thesis, University of Aberdeen, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252142.

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The aims of this thesis were to establish a suitable model system for the study of glucose and nutrient regulation of insulin secretion and biosynthesis. This would serve as a basis for investigating the GLP-1 effects on pancreatic b-cell biology. This thesis shows that two b-cell model systems, namely MIN6 and INS-1 cells, respond to increasing concentrations of glucose, by increasing insulin secretion and cell proliferation in a physiological manner. The MIN6 cell line also responds to other cellular nutrients, L-arginine and L-leucine in a manner similar to primary islet cells. The MIN6 cells however, fail to consistently increase insulin secretion in response to GLP-1, a known potentiator of insulin secretion in b-cells, despite the presence of the GLP-1 receptor. Incubation of GLP-1 with INS-1 cells, increases insulin secretion in a glucose-dependent manner, and causes a small increase in cell proliferation. GLP-1 is also known to increase cAMP levels within the cell and interact with cAMP response elements (CRE) via activation protein kinase A (PKA). Using a luciferase reporter gene construct containing 4 copies of the CRE, glucose, GLP-1 and forskolin failed to increase luciferase activity in MIN6 cells, suggesting that a defect in cAMP signalling may explain the inconsistent effect of GLP-1 in MIN6 cells. A stimulatory effect of GLP-1 and forskolin was observed in the INS-1 cells. Using both a rat insulin I and human insulin gene promoter construct, a stimulatory effect of GLP-1 on insulin gene transcription was observed in INS-1 cells. An insight into the signalling pathways involved in GLP-1 stimulation of the rat insulin I gene was gained through the use of protein kinase inhibitors, which inhibit signalling of known signal transduction cascades. It was found that an inhibitor of protein kinase A (H-89) was effective in blocking the increase in insulin promoter activity induced by GLP-1 using the rat insulin I promoter construct. Interestingly, the p38/SAPK2 inhibitor, SB203580, further increased the GLP-1 stimulation of rat insulin I promoter activity, indicating that this pathway usually invokes an inhibitory effect on insulin promoter activity.
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Lu, Jing. "Signalling and regulation of the glucagon-like peptide-1 receptor." Thesis, University of Leicester, 2014. http://hdl.handle.net/2381/28974.

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Following nutrient ingestion, glucagon-like peptide 1 (GLP-1) secreted from intestinal L-cells mediates anti-diabetic effects, most notably stimulating glucose-dependent insulin release from pancreatic β-cells but also inhibiting glucagon release, promoting satiety and weight reduction and potentially enhancing or preserving β-cell mass. These effects are through the GLP-1 receptor (GLP-1R) which is a therapeutic target in type 2 diabetes. The present study focused on desensitisation and re-sensitisation of GLP-1R-mediated signalling and interactions of orthosteric and allosteric ligands. Data demonstrate GLP-1R desensitisation and subsequent re-sensitisation following removal of extracellular ligand with ligand-specific features. Following GLP-1-mediated desensitisation, re-sensitisation is dependent on receptor internalisation, endosomal acidification and receptor recycling. Re-sensitisation is also dependent on endothelin converting enzyme-1 (ECE-1) activity, possibly through proteolysis of GLP-1 in endosomes, facilitating disassociation of receptor-β-arrestin complexes leading to GLP-1R recycling and re-sensitisation. ECE-1 activity also regulates GLP-1-induced activation of extracellular signal regulated kinase (ERK) and generation of cAMP possibly through a G protein independent/β-arrestin dependent mechanism. By contrast, following GLP-1R activation by the orthosteric agonist, exendin-4, or allosteric agonist, compound 2, re-sensitisation was slow and independent of ECE-1 activity. Thus, different ligands depend on different events during GLP-1R trafficking which could be important for re-sensitisation and signalling, particularly that mediated by scaffolding around β-arrestin. As the GLP-1R is targeted therapeutically at orthosteric and allosteric sites, this study examined activation of the GLP-1R by orthosteric and allosteric agonists and in particular interactions between ligands of these sites. Challenging the GLP-1R with the allosteric ligand, compound 2, along with GLP-1 9-36 amide, a low affinity, low efficacy metabolite of GLP-1 7-36 amide, results in synergistic receptor activation. This may be important for therapeutic approaches with allosteric ligands, as metabolites of GLP-1 may be present in vivo at concentrations higher than the classic endogenous ligand. Indeed this could present a novel therapeutic approach.
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KINZIG, KIMBERLY PEACOCK. "MULTIPLE ROLES OF THE CNS GLUCAGON-LIKE PEPTIDE-1 SYSTEM." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1037717933.

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Wishart, Clare. "The activation of the glucagon-like peptide-1 (GLP-1) receptor by peptide and non-peptide ligands." Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/5775/.

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The glucagon-like peptide-1 receptor (GLP-1R) potentiates glucose-stimulated insulin release from pancreatic β cells and promotes correct β cell function, as such it is a validated target for the treatment of type 2 diabetes (T2D). GLP-1R is a Family B GPCR, activated by the cognate ligand GLP-1(7-36), a 30 residue peptide hormone secreted after eating, and Exendin4 (Ex4), a 39-residue synthetic peptide. Peptide ligands interact with both the large extracellular domain and core domain of GLP-1R. Core domain interaction is thought to activate the receptor. Whilst the interaction between the receptor extracellular domain and ligand is well characterised, the ligand-core domain interaction and subsequent activation is not fully understood. Herein, a combination of mutant peptides and non-peptide ligands based on a pyrimidine scaffold (Pm compounds) are used in HTR-FRET cAMP accumulation assays, using recombinant FlpIn-HEK293 cells expressing human GLP-1R, to characterise the activation profiles of these ligands to decipher the underlying activation mechanism at the GLP-1R core domain. Structure-function studies of Pm compounds showed a trifluoromethyl and sulphur dioxide group are essential for GLP-1R activation, and that they allosterically enhance GLP-1(9-36) and Ex4(9-39) cAMP signalling profiles independently from their own cAMP response. Insulin secretion assays showed Pm compounds potentiate insulin release from INS-1 832/13 cells in combination with truncated GLP-1(9-36), implicating the use of allosteric modulators as treatment for T2D. Truncated GLP-1(15-36) was capable of binding and activating GLP-1R with low affinity and low potency, yet analogously truncated Ex4(9-39) was an antagonist with high affinity. Previous studies had demonstrated GLP-1(15-36) was an antagonist, and peptide-mediated activity had been attributed to the amino-terminus. Furthermore, the Pm compound-mediated cAMP response at GLP-1R was potentiated by Ex4(9-39). Mutant peptide activation data suggest activating residues D15, V16 and S17 are situated more centrally within the peptide ligand, and an extension to the currently accepted GLP-1R activation model is proposed.
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Books on the topic "Glucagon-like peptide 1"

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-C, Fehmann H., and Göke B. (Burkhard), eds. The insulinotropic gut hormone glucagon-like peptide-1. Basel: Karger, 1997.

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Joseph, Jamie William. Oral delivery of glucagon-like peptide-1 using PLGA-COOH microspheres. Ottawa: National Library of Canada, 1999.

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Kim, Julie. The roles of glucagon-like peptide-1 (GLP-1) in the mouse brain. Ottawa: National Library of Canada, 1998.

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Jeng, Winnie. Structural and functional studies of the glucagon-like peptide-1 (GLP-1) receptor. Ottawa: National Library of Canada, 1998.

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Sandhu, Harmanjit Singh. The effect of GLP-1, glucagon-like peptide 1, on insulin sensitivity in diabetic dogs. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Mendosa, David. Losing weight with your diabetes medication: How Byetta and other drugs can help you lose more weight than you ever thought possible. Philadelphia, PA: Da Capo Life Long, 2008.

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Cook, Sonya M. Characterization of mice with a null mutation in the glucagon-like peptide-1 receptro gene. Ottawa: National Library of Canada, 1998.

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Mendosa, David. Losing weight with your diabetes medication: How Byetta and other drugs can help you lose more weight than you ever thought possible. Philadelphia, PA: Da Capo Life Long, 2008.

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Satkunarajah, Malathy. Studies of the incretins, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, and their receptors. Ottawa: National Library of Canada, 1998.

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Green, Brian Desmond. Amino-terminally modified analogues of glucagon-like Peptide-1(7-36)Amide: Activity and antidiabetic potential. [S.l: The Author], 2003.

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Book chapters on the topic "Glucagon-like peptide 1"

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Tauber, R., and F. H. Perschel. "Glucagon-like peptide 1." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_1262-1.

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Tauber, R., and F. H. Perschel. "Glucagon-like peptide 1." In Springer Reference Medizin, 976–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1262.

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Gallwitz, Baptist. "Glucagon-like peptide-1 receptor agonists." In Handbook of Incretin-based Therapies in Type 2 Diabetes, 31–43. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-08982-9_3.

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Jeon, Ja Young, and Hae Jin Kim. "Glucagon-like Peptide-1 Receptor Agonists." In Stroke Revisited, 167–77. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-5123-6_14.

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Greenfield, Jerry R., and Dorit Samocha-Bonet. "Glutamine and Glucagon-Like Peptide-1 Response." In Glutamine in Clinical Nutrition, 277–91. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1932-1_21.

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Thorens, B., and C. Widmann. "Structure and Function of the Glucagon-Like Peptide-1 Receptor." In Glucagon III, 255–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61150-6_16.

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Alicic, Radica Z., Emily J. Cox, Joshua J. Neumiller, and Katherine R. Tuttle. "Glucagon-like Peptide-1 Receptor Agonists (GLP1-RA)." In Diabetes and Kidney Disease, 563–82. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-86020-2_26.

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Dillon, Joseph S., Michael B. Wheeler, Xing-Hong Leng, B. Brooke Ligon, and Aubrey E. Boyd. "The Human Glucagon-Like Peptide-1 (GLP-1) Receptor." In Advances in Experimental Medicine and Biology, 113–19. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1819-2_15.

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Bode, Hans-Peter, and Burkhard Göke. "Signal Transduction of GLP-1." In The Insulinotropic Gut Hormone Glucagon-Like Peptide-1, 142–51. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000194734.

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Göke, Burkhard. "Extrapancreatic Action of GLP-1." In The Insulinotropic Gut Hormone Glucagon-Like Peptide-1, 212–18. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000194738.

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Conference papers on the topic "Glucagon-like peptide 1"

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Ramos-Colon, Cyf, Andrew Kennedy, Daniel Martinez, and James Cain. "High-throughput parallel synthesis optimization of Glucagon-like Peptide 1 receptor agonists." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.110.

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Chandran, N., B. M. Nagy, E. Kathrin, W. Klepetko, G. Kwapiszewska, and A. Olschewski. "Role of Glucagon-Like Peptide -1 Receptor in Pulmonary Circulation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3673.

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Foer, D., T. Liu, T. Amin, S. Viswanathan, O. Boutaud, K. Cahill, and J. A. Boyce. "Glucagon-Like Peptide-1 Receptor Agonists Decrease Platelet-Mediated Airway Inflammation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1410.

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Rasouli, Mina, Zalinah Ahmad, Abdul Rahman Omar, Zeenathul Nazariah Allaudin, and Maznah Ismail. "Purification of Glucagon Like Peptide Purification of Glucagon Like Peptide--1 Expressing Cells from 1 Expressing Cells from Heterogeneous Population of Heterogeneous Population of Enteroendocrine Enteroendocrine Cell Line." In Annual International Conference on BioInformatics and Computational Biology & Annual International Conference on Advances in Biotechnology. Global Science and Technology Forum, 2011. http://dx.doi.org/10.5176/978-981-08-8119-1_biotech05.

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Huang, J. "Glucagon-Like Peptide-1 Receptor (GLP-1R) Signaling Ameliorates Dysfunctional Immunity in COPD Patients." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4525.

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Holfinger, Steven, Rashmeet Reen, William Ackerman, Douglas Kniss, and Keith J. Gooch. "PANC-1 Migration and Cluster Formation is Regulated by Short Range Mechanical Forces." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53593.

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Islet cell transplantation has already shown improved control of glucose levels and the potential to achieve insulin independence in type 1 diabetes mellitus, however there is a shortage of organ donors needed to match patient needs [1–2]. In the search for alternative sources of islets, many cell types have shown signs of β-cell differentiation by secreting c-peptide, insulin, and glucagon [3–5]. When maintained in serum-free medium, human epithelial-like pancreatic adenocarcinoma (PANC-1) cells and human-islet derived precursor cells (hIPCs) can go through a morphological transition and cluster [6]. These islet-like cell aggregates subsequently express glucagon, somatostatin, and insulin, indicating that clustering may play an important role in differentiation towards β-cells [7].
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Daly, J. M., Z. Yang, J. L. Ingram, K. M. Luginbuhl, A. Varanko, R. M. Tighe, A. Chilkoti, and L. G. Que. "Glucagon Like Peptide 1 Attenuates Airway Hyperresponsiveness in a Mouse Model of Obese Allergic Asthma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4424.

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Yuliawati, Alfi Taufik Fathurahman, Wien Kusharyoto, and Ratih Asmana Ningrum. "Construction of multicopy glucagon-like peptide-1 (GLP-1) open reading frame and its expression in Escherichia coli." In THE FIRST INTERNATIONAL CONFERENCE ON NEUROSCIENCE AND LEARNING TECHNOLOGY (ICONSATIN 2021). AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0118377.

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HASSAN, Neeran F. "USING INCRETIN IN TREATMENT OF DIABETES MELLITUS DISEASE." In IV.International Scientific Congress of Pure,Appliedand Technological Sciences. Rimar Academy, 2022. http://dx.doi.org/10.47832/minarcongress4-29.

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Incretin hormones are gut peptides secreted in response to nutrient ingestion, which play a key role in the regulation of islet function and blood glucose levels. In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose- dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect which is defined as the phenomenon whereby orally ingested glucose elicits a much greater insulin response than that obtained when glucose is infused intravenously to give identical blood glucose levels. there is evidence to suggest that impairments in secretion and/or action of incretin hormones arise secondarily to the development of insulin resistance, glucose intolerance, and/or increases in body weight rather than being causative factors. In separate studies, insulin sensitivity, glucose tolerance, and body mass index (BMI) have all been identified as independent factors associated with reductions in GLP-1 secretion and an impaired incretin effect. In patients with type 2 diabetes, the incretin effect is clearly reduced, which results in an inappropriately low insulin response to the ingestion of nutrients. Several early studies indicated that the reduced incretin effect could, at least in part, be related to impaired secretion of GLP- 1 (whereas secretion of GIP is generally found to be unaltered). Impaired meal-stimulated GLP-1 levels have been reported in some studies of patients with type 2 diabetes.  incretins exert antidiabetic actions in a glucose-dependent manner  Glucagon-like peptide 1 receptor (GLP-1r) agonists, but not dipeptidyl peptidase-4 (DPP-4) inhibitors, inhibit gastric emptying and might cause weight loss  DPP-4 inhibitors can be administered orally and are well tolerated  GLP-1r agonists must be administered by subcutaneous injection and commonly cause nausea. Key words: Incretin, Diabetes Mellitus..
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Foer, D., P. E. Beeler, J. Cui, E. Karlson, D. W. Bates, and K. Cahill. "Glucagon-Like Peptide-1 Receptor Agonist Use and Asthma Exacerbations Among Type 2 Diabetics with Asthma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2736.

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Reports on the topic "Glucagon-like peptide 1"

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Luan, Sisi, Wenke Cheng, Chenglong Wang, Hongjian Gong, and Jianbo Zhou. Impact of glucagon-like peptide 1 analogs on cognitive function among patients with type 2 diabetes mellitus. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0015.

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Review question / Objective: Diabetes is an independent risk factor for cognitive impairment. Little is known regarding the neuroprotective effects of glucagon-like peptide 1 (GLP-1) analogs on type 2 diabetes mellitus (T2DM).Here, the study aim to assess the impact of GLP-1 on general cognition function among patients with T2DM. Eligibility criteria: Inclusion criteria were as follows: (1) an original article was recently published in English, (2) the population included subjects diagnosed with diabetes at baseline, (3) GLP-1 analogs is a single formulation rather than a fixed dose combination, (4) GLP-1 analogs were compared with no GLP-1 use or placebo or self-control before treatment, (5) the duration of antidiabetic agent use was 12 weeks or more, and (6) it provided quantitative measures of general cognitive function assessed by MMSE or MoCA. Exclusion criteria were as follows: (1) the publication was a review, case report, animal study, or letter to the editor, (2) the study did not clearly define clinical outcomes, (3) the authors could not provide valid data after being contacted, (4) duplicated data.
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Zhuo, Chuanjun, Hongjun Tian, Lina Wang, Xiangyang Gao, Li Ding, and Ming Liu. Comparative safety of glucagon like peptide‑1 receptor agonists in patients with type 2 diabetes: a network meta-analysis of cardiovascular outcome trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0122.

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Deo, Salil, David McAllister, Naveed Sattar, and Jill Pell. The time-varying cardiovascular benefits of glucagon like peptide-1 agonist (GLP-RA)therapy in patients with type 2 diabetes mellitus: A meta-analysis of multinational randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0097.

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Review question / Objective: P - patients with type 2 diabetes melllitus already receiving routine medical therapy; I - patients receiving glucagon like peptide 1 receptor agonist (GLP1 receptor agonist) therapy (semaglutide, dulaglutide, liraglutide, exenatide, lixisenatide, efpeglenatide, abiglutide); C - patients receiving standard therapy for diabetes mellitus but not receiving GLP1 agonist therapy; O - composite end point as per invididual trial, cardiovascular mortality, all-cause mortality, myocardial infarction, stoke. Condition being studied: Type 2 diabetes mellitus. Study designs to be included: Randomised controlled trials which enroll a large number of patients (defined as > 500) and are multinational in origin. Studies included will need to have published Kaplan and Meier curves for the end-points presented in the manuscript.
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Xie, Yunhui, and Peng Pang. A Systematic Review and Network Meta-Analysis: Effect of of GLP-1 drugs on weight loss in obese people. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0074.

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Review question / Objective: 1、Whether GLP-1 drugs have weight loss effect on obese people ? 2、Which GLP-1 drugs are most effective in weight loss among obese people ? Condition being studied: Obesity is an important public health issue that has been on the rise over the last decades. It calls for effective prevention and treatment. Bariatric surgery is the most effective medical therapy for weight loss in morbid obesity, but we are in need for less aggressive treatments. Glucagon-like-peptide-1 receptor agonists are a group of incretin-based drugs that have proven to be productive for obesity treatment. Through activation of the GLP-1 receptor they not only have an important role stimulating insulin secretion after meals, but with their extrapancreatic actions, both peripheral and central, they also help reduce body weight by promoting satiety and delaying gastric emptying.
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