Готові списки джерел за темами / Glucagon-like peptide analogues

Добірка наукової літератури з теми "Glucagon-like peptide analogues"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Glucagon-like peptide analogues"

1

Zhang, Yifan, and Wengen Chen. "Radiolabeled glucagon-like peptide-1 analogues." Nuclear Medicine Communications 33, no. 3 (March 2012): 223–27. http://dx.doi.org/10.1097/mnm.0b013e32834e7f47.

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2

Gupta, Vishal. "Glucagon-like peptide-1 analogues: An overview." Indian Journal of Endocrinology and Metabolism 17, no. 3 (2013): 413. http://dx.doi.org/10.4103/2230-8210.111625.

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3

Nilsson, Peter M. "Hemodynamic effects by glucagon-like peptide-1 receptor analogues." Journal of Hypertension 35, no. 5 (May 2017): 953–54. http://dx.doi.org/10.1097/hjh.0000000000001315.

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4

Wilding, John P. H., and Kevin Hardy. "Glucagon-like peptide-1 analogues for type 2 diabetes." BMJ 342 (2011): d410. http://dx.doi.org/10.1136/bmj.d410.

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5

Chun, Hyun-Ji, and Hyuk-Sang Kwon. "Clinical Efficacy of Glucagon Like Peptide-1 (GLP-1) Analogues." Journal of Korean Diabetes 14, no. 3 (2013): 125. http://dx.doi.org/10.4093/jkd.2013.14.3.125.

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6

Gallwitz, Baptist. "Glucagon-like Peptide–1 Analogues for Type 2 Diabetes Mellitus." Drugs 71, no. 13 (September 2011): 1675–88. http://dx.doi.org/10.2165/11592810-000000000-00000.

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7

Dharmaraj, B. "A brief review on newer Glucagon like Peptide-1 analogues." International Journal of Preclinical and Clinical Research 1, no. 1 (December 21, 2020): 26–34. http://dx.doi.org/10.51131/ijpccr/v1i1.7.

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Анотація:
GLP-1 (Glucagon like Peptide-1) receptor agonists have been shown to be effective in the treatment of type 2 diabetes mellitus (T2DM). Although the first GLP-1 receptor agonist, Exenatide, was approved in the year 2000, other agents with a longer duration of action that do not require twice-daily dosing are now being developed. Indeed, Liraglutide, a once-daily GLP-1 receptor agonist, was approved in 2010, a once-weekly extended-release formulation of Exenatide (Exenatide ER) was approved in 2011 and now more recently Semaglutide, an oral GLP 1 receptor agonist was approved for medical use in the United States in September 2019 and in the European Union in April 2020. The importance of GLP-1 itself and the use of GLP-1 receptor agonists in T2DM are discussed. An overview of the clinical development of the GLP-1 receptor agonists (Exenatide ER, Liraglutide, Lixisenatide, Albiglutide, Taspoglutide and Semaglutide) is provided and their mechanism of action, efficacy in terms of glycaemic control, weight loss and tolerability are reviewed. Keywords: GLP1 receptor agonist; Liraglutide; Exenatide ER; Lixisenatide; Semaglutide
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8

Iacobellis, Gianluca. "Can epicardial fat glucagon-like peptide-1 receptor open up to the cardiovascular benefits of glucagon-like peptide-1 analogues?" Polish Archives of Internal Medicine 131, no. 3 (March 30, 2021): 224–25. http://dx.doi.org/10.20452/pamw.15904.

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Juul Holst, Jens. "Glucagon-like Peptide-1, A Gastrointestinal Hormone with a Pharmaceutical Potential." Current Medicinal Chemistry 6, no. 11 (November 1999): 1005–17. http://dx.doi.org/10.2174/092986730611220401163238.

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Glucagon-like peptide-1 (GLP-1) is an insulinotropic hormone secreted from endocrine cells in the gut mucosa in response to meal ingestion. It is an important incretin hormone; mice with a null mutation in the GLP-1 receptor gene develop glucose intolerance. In addition, it inhibits gastrointestinal secretion and motility and is thought to be part of the "ileal brake" mechanism. Perhaps because of the latter actions it inhibits food intake, but intracerebral injection of GLP-1 also inhibits food intake. The insu­ linotropic effect is preserved in patients with type 2 diabetes mellitus, in whom also glucagon secretion is inhibited. Thus upon iv GLP-1 infusion blood glucose may be completely normalised. Because its actions are glucose-dependent hypoglycaemia does not develop. However, GLP-1 is metabolised extremely rapidly in vivo, initially by a mechanism that involves the enzyme dipeptidyl peptidase-IV. It is currently being investigated how GLP-1 or analogues thereof can be employed in practical diabetes therapy. Promising solutions include the development of stable analogues and inhibitors of the degrading enzyme.
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10

Williams, David M., Matthew Staff, Stephen C. Bain, and Thinzar Min. "Glucagon-like Peptide-1 Receptor Analogues for the Treatment of Obesity." Endocrinology 18, no. 1 (2022): 43. http://dx.doi.org/10.17925/ee.2022.18.1.43.

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Анотація:
There is an increasing prevalence of obesity worldwide, associated with significant morbidity and mortality, which frequently reduces quality of life and life expectancy. Consequently, there is a substantial and growing personal and economic burden necessitating the development of more effective therapies for obesity. Glucagon-like peptide-1 receptor analogues (GLP-1RAs) are licensed for the treatment of type 2 diabetes (T2D), and there is substantial evidence that these drugs not only improve cardiovascular outcomes but also promote weight loss. More recent evidence supports the use of the GLP-1RAs liraglutide and semaglutide in people with obesity without T2D. This article discusses the results of the major cardiovascular outcome trials for GLP-1RAs in people with T2D, the SCALE Obesity and Prediabetes study (Effect of liraglutide on body weight in non-diabetic obese subjects or overweight subjects with co-morbidities: SCALE™ - Obesity and Pre-diabetes; ClinicalTrials.gov identifier: NCT01272219; investigating liraglutide) and the STEP studies (Semaglutide treatment effect in people with obesity; assorted studies; investigating subcutaneous semaglutide). We also highlight the importance of a cost-effective approach to obesity pharmacotherapy. Clinicians should consider the use of GLP-1RAs in people with obesity, especially those with T2D or other obesity-related diseases, such as hypertension and dyslipidaemia. Ongoing trials, as well as clinical and cost-effectiveness appraisals, are anticipated over the next 12 months, and their findings may change the current landscape of obesity pharmacotherapy.
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Більше джерел

Дисертації з теми "Glucagon-like peptide analogues"

1

Green, Brian Desmond. "Amino-terminally modified analogues of glucagon-like peptide-1 (7-36) amide : activity and antidiabetic potential." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398986.

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Fonseca, Filipa Ribeiro da. "Establishment of bioengineered glucose-responsive nanoparticles for type 2 diabetes mellitus therapy." Master's thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica António Xavier, 2019. http://hdl.handle.net/10362/130074.

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Dissertation presented to obtain the Master degree in Biochemistry for Health
"Type 2 diabetes mellitus (T2DM) is one of the biggest health problems in the world. Glucagon like peptide-1, an endogenous gastrointestinal incretin hormone that stimulates insulin secretion, is considered an attractive therapeutic agent for T2DM treatment. Nevertheless, its short half-life has led to the development of longer half-life GLP-1 analogues, as exenatide. Still, current dosage forms for exenatide delivery are not exempt of shortcomings. Nanotechnology-based systems may offer several advantages over conventional dosage forms for drug delivery.(...)"
N/A
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3

Bellman, Susan Marie. "The effectiveness of GLP-1 analogues compared to DPP-4 inhibitors for beta cell function and diabetes related complications among adults with type 2 diabetes: a systematic review and meta-analysis." Thesis, 2016. http://hdl.handle.net/2440/99884.

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Continued loss of beta cell function is responsible for progressive deterioration of plasma glucose control and complications characteristic of type 2 diabetes. Two classes of incretin-based antihyperglycaemic agents, dipeptidyl peptidase-4 (DPP-4) inhibitors and glucagon-like peptide-1(GLP-1) analogues, have shown favourable effects on beta cell function. The aim of this systematic review was to provide a comprehensive synthesis of randomised clinical studies comparing the effectiveness of GLP-1 analogues to DPP-4 inhibitors in improving beta cell function and managing diabetes related complications. A search of PubMed, EMBASE and national and international clinical trials databases was conducted for randomised controlled trials that compared GLP-1 analogues to DPP-4 inhibitors, either alone or in combination with metformin, in adults with type 2 diabetes. Methodological quality of included studies was assessed using the Joanna Briggs Institute (JBI) critical appraisal checklist, and research data was extracted using the JBI data extraction tool. Outcomes included beta cell function (measured by homeostasis model assessment-beta [HOMA-beta], plasma connecting peptide [C-peptide] and proinsulin to insulin [PI/I] plasma concentration ratio) glycated haemoglobin (HbA1c), fasting and postprandial plasma glucose levels, diabetes related complications, and adverse drug events. Seven randomised controlled trials including 2661 participants were included in this review. The overall quality of included studies was good. Treatment duration ranged from 24 to 52 weeks in the included studies and included a number of different dosages. Results of meta-analysis showed that GLP-1 analogues, at different dosages and duration, were associated with statistically significant improvements in beta cell function compared to DPP-4 inhibitors as measured by HOMA-beta; mean difference 23% and 25% for high dose GLP-1 analogues after 26 and 52 weeks, respectively (p<0.00001); 18.5% and 16.7% for low dose GLP-1 analogues after 26 and 52 weeks, respectively (p<0.00001). Treatment with GLP-1 analogues showed a greater reduction in glycated haemoglobin (HbA1c) compared to treatment with DPP-4 inhibitors: a mean difference of -0.52% and -0.68% (-5.67mmol/moL and - 7.41mmol/moL) for high dose GLP-1 analogues after 26 and 52 weeks, respectively (p<0.00001); and -0.38% and -0.45% (-4.14mmol/moL and -4.91mmol/moL) for low dose GLP- 1 analogues after 26 and 52 weeks, respectively (p<0.00001). Treatment with GLP-1 analogues resulted in a greater reduction in fasting plasma glucose compared to DPP-4 inhibitors: a mean difference of -1.23 mmol/L and -1.47 mmol/L (-22.16 mg/dL and -26.49 mg/dL) for high dose GLP-1 analogues after 26 and 52 weeks, respectively p<0.00001); and -1.01mmol/L and -0.84mmol/L (-18.20mg/dL and -15.13 mg/dL) for low dose GLP-1 analogues after 26 and 52 weeks, respectively (p<0.00001). No studies reported outcomes for diabetes related complications. However, DPP-4 inhibitors were associated with fewer gastrointestinal adverse events compared to GLP-1 analogues. There were no differences in other adverse events such as headache and infection. The findings showed that GLP-1 analogues had greater beneficial effects on pancreatic beta cell function and plasma glucose control than DPP-4 inhibitors, but caused more gastrointestinal adverse events. Longer term safety data is required to better identify the contribution of GLP-1 analogues in reducing diabetes related microvascular complications, and determine their long term pancreatic and cardiac effects.
Thesis (M.Clin.Sc.) -- University of Adelaide, Joanna Briggs Institute, 2016.
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4

Araújo, Ana Francisca Lopes Correia de. "Glucagon-like peptide-1 and glucagon-like peptide-1 analogs nanotechnology-based systems for prevention and therapy of diabetes." Doctoral thesis, 2017. https://repositorio-aberto.up.pt/handle/10216/103191.

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Araújo, Ana Francisca Lopes Correia de. "Glucagon-like peptide-1 and glucagon-like peptide-1 analogs nanotechnology-based systems for prevention and therapy of diabetes." Tese, 2017. https://repositorio-aberto.up.pt/handle/10216/103191.

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6

Liu, Hsien-Yueh, and 劉獻岳. "Exendin-4, a glucagon-like peptide-1 analogue, improves Listeria monocytogenes infection in diabetic db/db mice." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/89597295148737323856.

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博士
國立中興大學
獸醫學系暨研究所
103
This diabetes mellitus has similar characteristics in both humans and animals. The incidence of this disease is increasing among companion animals. Diabetes is frequently identified as an independent risk factor for infections associated with increased mortality. In this study, homozygous diabetic (db/db) mice were infected with Listeria monocytogenes and then treated with the diabetic treatment drug Exendin-4, a glucagon-like peptide 1 analogue. In aged db/db mice, decreased CD11b+ macrophage populations with higher lipid content and lower phagocytic activity were observed. Exendin-4 lowered high lipid levels and enhanced phagocytosis in macrophages from db/db mice infected with L. monocytogenes. Exendin-4 also ameliorated obesity and hyperglycemia, and improved ex vivo bacteria clearance by macrophages in the diabetic animals. Liver histology examined during L. monocytogenes infection indicated that abscess formation was much milder in Exendin-4 treated db/db mice than in the control animals. Moreover, the expression of ATP binding cassette transporter 1, a sterol transporter, in the macrophages isolated from the Exendin-4 treated db/db mice was higher than the untreated group. Overall, our results indicated that Exendin-4 reduces the risk of infection in diabetic animals by modulating the interaction between intracellular lipids and phagocytic ability of macrophages
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Книги з теми "Glucagon-like peptide analogues"

1

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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Частини книг з теми "Glucagon-like peptide analogues"

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Dong, Jesse Z., Yeelana Shen, John E. Taylor, Michael Culler, Chee-Wai Woon, Barry Morgan, Steve Skinner, and Jacques-Pierre Moreau. "Glucagon-Like Peptide-1 Analogs with Significantly Improved in vivo Activity." In Peptides: The Wave of the Future, 670–71. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_312.

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2

Li, Hongjian, Cindy X. Zhou, and Zhengding Su. "Protease-resistant glucagon like peptide-1 analogs with long-term anti-diabetes type 2 activity." In Advances in Experimental Medicine and Biology, 475–76. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-73657-0_204.

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3

Kumar, Ajay. "Glucagon-like Peptide-1 Analogues." In Diabetology: Type 2 Diabetes Mellitus, 87. Jaypee Brothers Medical Publishers (P) Ltd., 2014. http://dx.doi.org/10.5005/jp/books/12165_8.

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4

Kumar, Ajay. "Chapter-08 Glucagon-like Peptide-1 Analogues." In Challenging and Rare Cases in Urology, 87–104. Jaypee Brothers Medical Publishers (P) Ltd., 2014. http://dx.doi.org/10.5005/jp/books/12153_8.

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5

Middleton, Stephen J., Simon M. Gabe, and Raymond J. Playford. "Effects of massive bowel resection." In Oxford Textbook of Medicine, edited by Jack Satsangi, 2911–16. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0304.

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Анотація:
Major vascular events involving the superior mesenteric artery and small-bowel volvulus are the commonest reasons for adults to require massive intestinal resection. The ability of the residual bowel to adapt after resection varies greatly between patients, but common postoperative problems include sepsis, diarrhoea (or high-output stoma losses), fluid and electrolyte imbalance, malnourishment (protein–energy malnutrition, mineral and vitamin deficiencies), gallstones, renal stones, and psychological illness. Where appropriate, oral nutrition, initially consisting of low-volume polymeric feeds administered by nasogastric or enteral tube, should be started within the first few days of surgery. Small-volume, frequent, solid or semisolid meals with low long-chain triglycerides and (when colon is in continuity) oxalate content should be introduced subsequently, and isotonic electrolyte solutions given as required. Oral multivitamin and mineral supplements are usually needed, and vitamin B12 injections may be required. There should be regular long-term monitoring of fat-soluble vitamins (A and D), vitamin B12, folate, magnesium, zinc, and bone status. Long-term intravenous nutrition is sometimes needed. Growth factor administration, especially glucagon-like peptide-2 analogues, may stimulate bowel adaptation. Small-bowel lengthening may be considered for patients with dilated bowel close to the length required. Those who are dependent on peripheral nutrition and develop complications such as loss of venous access or liver disease should be considered for intestinal transplantation.
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6

Deshpande, Neeta, and Pooja Kulkarni. "Glucagon-like Peptide-1 Analogs for Obesity Management." In RSSDI Diabetes Update 2016, 371. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13026_68.

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7

Diz-Chaves, Yolanda, Salvador Herrera-Pérez, Lucas C. González-Matías, and Federico Mallo. "Effects of Glucagon-like peptide 1 (GLP-1) analogs in the hippocampus." In Vitamins and Hormones. Elsevier, 2022. http://dx.doi.org/10.1016/bs.vh.2021.12.005.

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8

Pei, Zhe, Kuo-Chieh Lee, Amber Khan, and Hoau-Yan Wang. "Brain Insulin Resistance, Nitric Oxide and Alzheimer’s Disease Pathology." In The Role of Nitric Oxide in Type 2 Diabetes, 238–59. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010014.

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Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by progressive pathological changes and functional and cognitive impairments. Brain insulin resistance appears to contribute significantly to the pathology and cognitive deficits among several pathological mechanisms. Brain insulin resistance has been demonstrated in animal models of AD and postmortem human brain tissue from patients with AD dementia. Studies conducted in AD models and humans suggest attenuating brain insulin resistance by agents such as glucagon-like peptide1 (GLP-1) analogs and small molecule drug candidate PTI-125 reduces many AD pathologic features and symptoms. Insulin affects NO levels by activating endothelial and neuronal nitric oxide synthase (eNOS, nNOS), and systemic insulin resistance has been linked to reduced nitric oxide (NO) bioavailability. Increasing NO availability reduces systemic insulin resistance, and the insulin signaling pathway is associated with the activation of eNOS, implying a causal relationship. This chapter explores this relationship and the role of impaired NO availability in brain insulin resistance in AD dementia.
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Тези доповідей конференцій з теми "Glucagon-like peptide analogues"

1

Abudalo, Rawan, Kevin Edgar, Karla O’Neill, David Grieve, and Brian Green. "146 Glucagon-like peptide-1 analogues exert differential in vitro actions on macrophages and cardiac fibroblasts in experimental diabetes." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.142.

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Звіти організацій з теми "Glucagon-like peptide analogues"

1

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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