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Academic literature on the topic 'Incretin hormones'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Incretin hormones"

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Shah, Faraaz Ali, Hussain Mahmud, Teresa Gallego-Martin, Michael J. Jurczak, Christopher P. O’Donnell, and Bryan J. McVerry. "Therapeutic Effects of Endogenous Incretin Hormones and Exogenous Incretin-Based Medications in Sepsis." Journal of Clinical Endocrinology & Metabolism 104, no. 11 (June 19, 2019): 5274–84. http://dx.doi.org/10.1210/jc.2019-00296.

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Abstract Background Sepsis, a complex disorder characterized by a dysregulated immune response to an inciting infection, affects over one million Americans annually. Dysglycemia during sepsis hospitalization confers increased risk of organ dysfunction and death, and novel targets for the treatment of sepsis and maintenance of glucose homeostasis are needed. Incretin hormones are secreted by enteroendocrine cells in response to enteral nutrients and potentiate insulin release from pancreatic β cells in a glucose-dependent manner, thereby reducing the risk of insulin-induced hypoglycemia. Incretin hormones also reduce systemic inflammation in preclinical studies, but studies of incretins in the setting of sepsis are limited. Methods In this bench-to-bedside mini-review, we detail the evidence to support incretin hormones as a therapeutic target in patients with sepsis. We performed a PubMed search using the medical subject headings “incretins,” “glucagon-like peptide-1,” “gastric inhibitory peptide,” “inflammation,” and “sepsis.” Results Incretin-based therapies decrease immune cell activation, inhibit proinflammatory cytokine release, and reduce organ dysfunction and mortality in preclinical models of sepsis. Several small clinical trials in critically ill patients have suggested potential benefit in glycemic control using exogenous incretin infusions, but these studies had limited power and were performed in mixed populations. Further clinical studies examining incretins specifically in septic populations are needed. Conclusions Targeting the incretin hormone axis in sepsis may provide a means of not only promoting euglycemia in sepsis but also attenuating the proinflammatory response and improving clinical outcomes.
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Green, Brian D., Clifford J. Bailey, and Peter R. Flatt. "Gliptin Therapies for Inhibiting Dipeptidyl Peptidase-4 in Type 2 Diabetes." European Endocrinology 6, no. 2 (2010): 19. http://dx.doi.org/10.17925/ee.2010.06.02.19.

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Discovery of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) has led to the clinical development of incretin-based therapies for type 2 diabetes. Incretins are intestinal peptide hormones that stimulate post-prandial insulin secretion and improve glycaemic control. Gliptins are drugs that inhibit a ubiquitous enzyme, dipeptidyl peptidase-4 (DPP-4), preventing the physiological breakdown of incretins and thereby enhancing endogenous incretin action. Three ‘gliptins’ have recently been introduced into clinical practice: sitagliptin, vildagliptin and saxagliptin. This review provides an overview of these new antidiabetic agents and comments on some exciting future prospects for incretins and agents that enhance incretin action.
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Tsygankova, Oksana V., Varvara V. Veretyuk, and Alexander S. Ametov. "Incretins today: multiple effects and therapeutic potential." Diabetes mellitus 22, no. 1 (April 8, 2019): 70–78. http://dx.doi.org/10.14341/dm9841.

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Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) are the incretin hormones initially discovered in the 1960s. GIP and GLP-1 have gained great scientific interest due to their properties in increasing insulin secretion and lowering blood glucose levels. The study of these incretin hormones has progressed substantially in recent decades, in that their systemic effects has begun to be actively discussed. In particular, incretins are involved in the pathogenesis of obesity and non-alcoholic fatty liver disease. Moreover, incretins are able to improve cognitive function, suppress the formation of -amyloid plaques and provide an oncoprotective effect. Recent data show promising oncoprotective effect of GLP-1 agonists on prostate and breast cancer. This review provides systematisation of recent data on the role and mechanisms of action of incretin hormones on carbohydrate metabolism, as well as effects not related to glucose homeostasis, which contributes to a better understanding of potential vectors for the development of incretinotropic therapy. In addition, this review offers insight into pathogenic prerequisites and highlights the current issues in creating innovative polyagonists for treatment of type 2 diabetes mellitus.
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Michałowska, Joanna, Ewa Miller-Kasprzak, and Paweł Bogdański. "Incretin Hormones in Obesity and Related Cardiometabolic Disorders: The Clinical Perspective." Nutrients 13, no. 2 (January 25, 2021): 351. http://dx.doi.org/10.3390/nu13020351.

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The prevalence of obesity continues to grow rapidly worldwide, posing many public health challenges of the 21st century. Obese subjects are at major risk for serious diet-related noncommunicable diseases, including type 2 diabetes mellitus, cardiovascular disease, and non-alcoholic fatty liver disease. Understanding the mechanisms underlying obesity pathogenesis is needed for the development of effective treatment strategies. Dysregulation of incretin secretion and actions has been observed in obesity and related metabolic disorders; therefore, incretin-based therapies have been developed to provide new therapeutic options. Incretin mimetics present glucose-lowering properties, together with a reduction of appetite and food intake, resulting in weight loss. In this review, we describe the physiology of two known incretins—glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and their role in obesity and related cardiometabolic disorders. We also focus on the available and incoming incretin-based medications that can be used in the treatment of the above-mentioned conditions.
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Deacon, CF, S. Wamberg, P. Bie, TE Hughes, and JJ Holst. "Preservation of active incretin hormones by inhibition of dipeptidyl peptidase IV suppresses meal-induced incretin secretion in dogs." Journal of Endocrinology 172, no. 2 (February 1, 2002): 355–62. http://dx.doi.org/10.1677/joe.0.1720355.

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The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are degraded by dipeptidyl peptidase IV (DPP IV), thereby losing insulinotropic activity. DPP IV inhibition reduces exogenous GLP-1 degradation, but the extent of endogenous incretin protection has not been fully assessed, largely because suitable assays which distinguish between intact and degraded peptides have been unavailable. Using newly developed assays for intact GLP-1 and GIP, the effect of DPP IV inhibition on incretin hormone metabolism was examined. Conscious dogs were given NVP-DPP728, a specific DPP IV inhibitor, at a dose that inhibited over 90% of plasma DPP IV for the first 90 min following treatment. Total and intact incretin concentrations increased (P<0.0001) following a mixed meal, but on control days (vehicle infusion), intact peptide concentrations were lower (P<0.01) than total peptide concentrations (22.6 +/- 1.2% intact GIP; 10.1 +/- 0.4% intact GLP-1). Following inhibitor treatment, the proportion of intact peptide increased (92.5 +/- 4.3% intact GIP, P<0.0001; 99.0 +/- 22.6% intact GLP-1, P<0.02). Active (intact) incretins increased after NVP-DPP728 (from 4797 +/- 364 to 10 649 +/- 106 pM x min for GIP, P<0.03; from 646 +/- 134 to 2822 +/- 528 pM x m in for GLP-1, P<0.05). In contrast, total incretins fell (from 21 632 +/- 654 to 12 084 +/- 1723 pM x min for GIP, P<0.002; from 5145 +/- 677 to 3060 +/- 601 pM x min for GLP-1, P<0.05). Plasma glucose, insulin and glucagon concentrations were unaltered by the inhibitor. We have concluded that DPP IV inhibition with NVP-DPP728 prevents N-terminal degradation of endogenous incretins in vivo, resulting in increased plasma concentrations of intact, biologically active GIP and GLP-1. Total incretin secretion was reduced by DPP IV inhibition, suggesting the possibility of a feedback mechanism.
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Ørskov, Jens Juul Holst, Cathrine. "Incretin hormones - an update." Scandinavian Journal of Clinical and Laboratory Investigation 61, no. 234 (January 2001): 75–85. http://dx.doi.org/10.1080/clb.61.234.75.85.

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Holst, Jens Juul, and Cathrine Ørskov. "Incretin hormones - an update." Scandinavian Journal of Clinical and Laboratory Investigation 61, no. 7 (November 10, 2001): 75–85. http://dx.doi.org/10.1080/713783697.

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Phillips, Liza K., and Johannes B. Prins. "Update on incretin hormones." Annals of the New York Academy of Sciences 1243, no. 1 (December 2011): E55—E74. http://dx.doi.org/10.1111/j.1749-6632.2012.06491.x.

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Efendic, S., and N. Portwood. "Overview of Incretin Hormones." Hormone and Metabolic Research 36, no. 11/12 (November 2004): 742–46. http://dx.doi.org/10.1055/s-2004-826157.

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Holst, Jens Juul, and Cathrine Ørskov. "Incretin hormones – an update." Scandinavian Journal of Clinical and Laboratory Investigation 61, no. 7 (November 10, 2001): 75–85. http://dx.doi.org/10.1080/003655101317095455.

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Dissertations / Theses on the topic "Incretin hormones"

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Baggio, Laurie L. "The role of incretin hormones in glucose homeostasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ59004.pdf.

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Edholm, Therese. "The role of incretin peptides and ghrelin in upper gut motility and metabolic control /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-937-8/.

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Moss, Catherine Elizabeth. "G-protein coupled receptors modulating incretin hormone secretion." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648611.

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McCool, Katherine E. "The effect of diet and adiposity on the secretion of incretin hormones in cats." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1471605344.

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Joo, Erina. "The effects of nutrition intake on intestinal mucosal repair and metabolic regulation through gut hormones." Kyoto University, 2014. http://hdl.handle.net/2433/188804.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第18366号
人博第679号
新制||人||163(附属図書館)
25||人博||679(吉田南総合図書館)
31224
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授 林 達也, 教授 森谷 敏夫, 教授 石原 昭彦, 教授 津田 謹輔
学位規則第4条第1項該当
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Parker, Helen Elizabeth. "Mechanisms underlying nutrient stimulated incretin hormone secretion." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608858.

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Habib, A. M. "Properties of incretin hormone secreting cells : a primary cells study." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599820.

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Incretins GLP-1 and GIP are glucose regulating peptides released from L cells and K cells in the intestine in response to food intake. They act on pancreatic β-cells to potentiate glucose-stimulated insulin release. However, incretins also play a role in regulating body weight: GLP-1 promotes weight loss by acting as a satiety signal, whereas GIP is associated with weight gain by promoting adiposity. The association between incretins and obesity/diabetes highlights the need to identify physiological signals that control their release; however this has been hampered because of our lack of a handle on these cells. Here, we report that using tissues from transgenic mice with L cell-specific or K cell-specific expression of a fluorescent protein, these rare cell populations can be highly purified and changes in their total number and/or gene expression profile (e.g. in obesity) can be monitored by FACS and quantitative RT-PCR. We have developed a cell culture system to maintain L cells and K cells in vitro. This system is suitable to characterize these cells by electrophysiology, calcium imaging, hormone secretion studies and these cells are conducive to adenoviral transfection. Affymetrix based comparative global gene expression profiles indicated that L cells from the small intestine share more commonality to K cells than to L cells in the colon. Furthermore, we have identified a number of candidate sensors for dietary fatty acids, amino acids or glucose as well as signalling pathways preferentially expressed in L cells and/or K cells. A better understanding of these genes and pathways may help us to determine how the levels of these important hormones can be modulated in patients with type 2 diabetes and obesity.
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Fernandes, Gustavo. "Avaliação do metabolismo glicêmico e perfil entero-hormonal no pós-operatório precose em pacientes abesos graves diabéticos submetidos à gastroplastia em Y de Roux.Comparação da oferta alimentar por via oral e por gastrostomia." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5168/tde-29112017-091214/.

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INTRODUÇÃO: O diabetes mellitus tipo 2 (DM2) é uma doença correlacionada com a obesidade mórbida. O paciente obeso apresenta efeito incretínico suprimido e consequente desbalanço da homeostase glicêmica. Diversos estudos evidenciam a melhora do DM2 após a confecção da Gastroplastia com derivação intestinal em Y de Roux (GDYR). Os mecanismos de controle da glicemia podem ser de longo e curto prazo. Os mecanismos de ação precoce estão ligados à restrição calorica, melhora da resistência insulínica, da função da célula beta pancreática e retorno do efeito incretínico pelo aumento do GLP1 e GIP, porém os dados são conflitantes. MÉTODOS: Onze pacientes obesos graves diabéticos foram submetidos à GDYR com confecção de gastrostomia no remanescente gástrico após perda de peso inicial de 10%. Os pacientes foram submetidos à coleta de entero-hormônios, perfil glicêmico e Teste de Tolerância Oral à glicose (TTOG) no pré-operatório em curva temporal que foi comparado ao pós-operatório por Via Oral e por Via da Gastrostomia em até 7 dias após o procedimento. RESULTADOS: A média da idade foi 46,09±7,08 anos. No pré-operatorio, o peso médio foi 120,97±17,02 quilogramas, altura 1,67±0,11 metros, IMC médio 44,06±6,59 kg/m2, glicemia de jejum média 194,55±62,45 mg/dl e hemoglobina glicada 8,74±1,64%. Em 77,7% dos pacientes, houve remissão precoce do DM2 no pós-operatório avaliado pelo TTOG. Também foi observada queda significante da glicemia, insulinemia e do HOMA-IR independente da via administrada. Ocorreu aumento significativo do GLP1 e redução do GIP pela Via Oral pós-operatória. A Grelina não apresentou alterações. CONCLUSÃO: Evidenciou-se redução da glicemia e da resistência periférica nos primeiros dias de pós-operatório da GDYR, independente da via de passagem do alimento. A alteração no efeito incretínico (aumento do GLP1 e redução do GIP) só foi observada na Via Oral pós-operatória
INTRODUCTION: Type 2 diabetes mellitus (DM2) is a disease correlated with morbidly obesity. The obese patient has a suppressed incretin effect and consequent inbalance of glycemic homeostasis. Several studies have shown an improvement in DM2 after Gastroplasty with Roux-en-Y gastric bypass (RYGB). The mechanisms of glycemic control may be long-term and shortterm. The mechanisms of early action are linked to caloric restriction, improvement of insulin resistance, pancreatic beta cell function and return of the incretin effect through the increase of GLP1 and GIP, but the data are conflicting. METHODS: Eleven diabetic obese patients underwent RYGB with gastrostomy in gastric remnant after initial 10% weight loss. Patients were submitted to assessment of enterohormones, glycemic profile and Oral Glucose Tolerance Test (OGTT) in the preoperative period in a time curve that was compared to the postoperative period by Oral Via and Gastrostomy Via up to 7 days after the procedure .RESULTS: The mean age of the group was 46.09 ± 7.08 years. In the preoperative the mean weight was 120.97 ± 17.02 kilograms, height of 1.67 ± 0.11 meters, mean BMI of 44.06 ± 6, 59 kg/m2, mean fasting blood glucose of 194.55 ± 62.45 mg/dl and glycated hemoglobin 8.74 ± 1.64%. In 77.7% of the patients there was remission of DM2 in postoperative evaluated by the OGTT. Significant decrease in glycemia, insulinemia and HOMA-IR was also observed, regardless of the route of administration. There was a significant increase in GLP1 and reduction of GIP by the postoperative oral route. Ghrelin did not change. CONCLUSION: A reduction in glycemia and peripheral insulinal resistance was observed in early postoperative days of RYGB, independent of the food route. The change in incretin effect (increase of GLP1 and reduction of GIP) was only observed in the postoperative oral route
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Abdullahi, Mohamed Mohamed. "GLP-1 REGULATES PROLIFERATION OF GLP-1 SECRETING CELLS THROUGH A FEEDBACK MECHANISM." Thesis, Mälardalen University, School of Sustainable Development of Society and Technology, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-9756.

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Abstract

Background and aim:

Diabetes mellitus (DM) is a chronic and progressive illness that affects all type of populations and ages. According to World health organization (WHO) by 2030 it will be 366 million people effected world wild. Many new drugs are Glucagon-like peptide-1 (GLP-1) based therapy for treatment of type 2diabetes. GLP-1 is released from the intestinal L-cells, and is a potent stimulator of glucose-dependent insulin secretion. The aim of this study was to investigate the effect of GLP-1 and its stable analogs on cell proliferation of GLP-1 secreting GLUTag cells.

Material and methods:

GluTag cells were incubated for 48h in DMEM medium containing (0.5% fetal bovine serum and 100 IU/ml penicillin and 100 μg/ml streptomycin and 3mM glucose concentration) in the present or absence of the agents. DNA synthesis was measured using 3H- thymidine incorporation and Ki67 antigen staining. Western blot were performed to investigate the present of GLP-1 receptor in GLUTag cells.

Results/conclusions:

These results suggest that GLP-1 regulates proliferation of the GLP-1-secreting cell through a feedback mechanism via its receptor. Since serum GLP-1 levels are decreased in type 2 diabetic patients, the effect of GLP-1 on the GLP-1-secreting cell proliferation suggested here provides a novel beneficial long-term effect of the incretin-based drugs in clinical practice i.e. through increase of the GLP-1-secreting cell mass, augmenting the incretin effect. In addition, the feedback mechanism action of GLP-1 reveals a new insight in regulation manner of the L-cell proliferation.

GLP-1(7-36) increased cell proliferation in GLUTag cells, an effect which was blocked by the GLP-1 receptor antagonist exendin(9-39). The GLP-1 receptor was expressed in GluTag cells.

Keywords:

Incretin hormone, GLP-1, GLP-1 receptor, Exendin-4, Diabetes

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Lu, Wendell J. "Role of Macronutrients in the Regulation and Secretory Mechanisms of Gastrointestinal Hormones, Glucagon-like Peptide-1 (GLP-1) and Glucose-dependent Insulinotropic Polypeptide (GIP), in Lymph." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204084153.

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Books on the topic "Incretin hormones"

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Liu, Hui-Kang. Modification of the function of insulin-secreting cells by beta-cell toxins, differentiation drugs, insulin mimetics, steriods, and incretin hormones and their stable analogues. [S.l: The Author], 2003.

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Baggio, Laurie L. The role of incretin hormones in glucose homeostasis. 2001.

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Hansotia, Tanya. Elucidating novel biological actions of the incretin hormones GLP-1 and GIP. 2006.

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Book chapters on the topic "Incretin hormones"

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Holst, Jens Juul. "Incretin hormones as a target for therapy." In Handbook of Incretin-based Therapies in Type 2 Diabetes, 11–30. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-08982-9_2.

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De León, Diva D. "Role of Incretin Hormones in Hyperinsulinemic Hypoglycemia." In Monogenic Hyperinsulinemic Hypoglycemia Disorders, 79–86. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000334509.

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Thorens, Bernard. "The GIuco-Incretin Hormone Glucagon-Like Peptide-1 and Its β-Cell Receptor." In Molecular Biology of Diabetes, 357–79. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4612-0241-7_15.

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C, Shivaprasad. "Incretin Hormones: Effects Beyond Glycemic Control." In Incretin Based Therapies, 18. Jaypee Brothers Medical Publishers (P) Ltd., 2013. http://dx.doi.org/10.5005/jp/books/11892_3.

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McIntosh, Christopher H. S., Scott Widenmaier, and Su-Jin Kim. "Pleiotropic Actions of the Incretin Hormones." In Incretins and Insulin Secretion, 21–79. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-381517-0.00002-3.

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Zietek, Tamara, Nadine Waldschmitt, and Eva Rath. "Role of Incretin Hormones in Bowel Diseases." In Developmental Biology of Gastrointestinal Hormones, 49–73. S. Karger AG, 2017. http://dx.doi.org/10.1159/000475731.

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Irwin, David M. "Evolution of Genes for Incretin Hormones and their Receptors." In Incretins and Insulin Secretion, 1–20. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-381517-0.00001-1.

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Holscher, Christian. "Protective Roles of the Incretin Hormones Glucagon-Like Peptide-1 and Glucose-Dependent Insolinotropic Polypeptide Hormones in Neurodegeneration." In Alzheimer's Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets. InTech, 2011. http://dx.doi.org/10.5772/18372.

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"The Incretin Effect: Regulation of Insulin Secretion and Glucose Tolerance by GI Hormones." In Diabetes, 135–50. CRC Press, 2008. http://dx.doi.org/10.3109/9781420047363-10.

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"Incretin Hormone." In Encyclopedia of Signaling Molecules, 2585. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_105325.

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Conference papers on the topic "Incretin hormones"

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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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Kartono, Agus, Rojali Fadila, Heryanto Syafutra, Setyanto Tri Wahyudi, and Tony Sumaryada. "The Modified Oral Minimal Model to Know Incretin Hormone Effect in Type 2 Diabetes Mellitus." In The 7th Engineering International Conference (EIC), Engineering International Conference on Education, Concept and Application on Green Technology. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0009009802800286.

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Kartono, Agus, Rojali Fadila, Heryanto Syafutra, Setyanto Tri Wahyudi, and Tony Sumaryada. "The Modified Oral Minimal Model to Know Incretin Hormone Effect in Type 2 Diabetes Mellitus." In The 7th Engineering International Conference (EIC), Engineering International Conference on Education, Concept and Application on Green Technology. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0009009802860292.

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