Relevant bibliographies by topics / Exenatide (exendin-4)

Academic literature on the topic 'Exenatide (exendin-4)'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Exenatide (exendin-4)"

1

Wei, Rui, Shifeng Ma, Chen Wang, Jing Ke, Jin Yang, Weihong Li, Ye Liu, et al. "Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner." American Journal of Physiology-Endocrinology and Metabolism 310, no. 11 (June 1, 2016): E947—E957. http://dx.doi.org/10.1152/ajpendo.00400.2015.

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Glucagon-like peptide-1 (GLP-1) may have direct favorable effects on cardiovascular system. The aim of this study was to investigate the effects of the GLP-1 analog exenatide on improving coronary endothelial function in patients with type 2 diabetes and to investigate the underlying mechanisms. The newly diagnosed type 2 diabetic subjects were enrolled and given either lifestyle intervention or lifestyle intervention plus exenatide treatment. After 12-wk treatment, coronary flow velocity reserve (CFVR), an important indicator of coronary endothelial function, was improved significantly, and serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were remarkably decreased in the exenatide treatment group compared with the baseline and the control group. Notably, CFVR was correlated inversely with hemoglobin A1c (Hb A1c) and positively with high-density lipoprotein cholesterol (HDL-C). In human umbilical vein endothelial cells, exendin-4 (a form of exenatide) significantly increased NO production, endothelial NO synthase (eNOS) phosphorylation, and GTP cyclohydrolase 1 (GTPCH1) level in a dose-dependent manner. The GLP-1 receptor (GLP-1R) antagonist exendin (9–39) or GLP-1R siRNA, adenylyl cyclase inhibitor SQ-22536, AMPK inhibitor compound C, and PI3K inhibitor LY-294002 abolished the effects of exendin-4. Furthermore, exendin-4 reversed homocysteine-induced endothelial dysfunction by decreasing sICAM-1 and reactive oxygen species (ROS) levels and upregulating NO production and eNOS phosphorylation. Likewise, exendin (9–39) diminished the protective effects of exendin-4 on the homocysteine-induced endothelial dysfunction. In conclusion, exenatide significantly improves coronary endothelial function in patients with newly diagnosed type 2 diabetes. The effect may be mediated through activation of AMPK/PI3K-Akt/eNOS pathway via a GLP-1R/cAMP-dependent mechanism.
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2

Zhang, Aihong, Yin Lin, Shirly Nong, Wei Zhao, and Mei Dong. "Engineering a protease-based and site-specific PEGylation-based strategy for the controlled release of exenatide." RSC Advances 10, no. 42 (2020): 25013–21. http://dx.doi.org/10.1039/d0ra01010c.

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Using the commercially available antidiabetic drug exenatide (exendin-4) as a model peptide, we designed a novel exenatide derivative, termed LEX-1, comprising a 12-mer albumin-binding peptide, a protease-sensitive linker and a native exenatide.
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3

Zhao, Qian, Chun-ling Xu, Hai-yan Xiong, Wen Huang, Mei Zhang, Yun Wang, Si-yu Wang, and Wen Wang. "Alleviation of Hyperglycemia Induced Vascular Endothelial Injury by Exenatide Might Be Related to the Reduction of Nitrooxidative Stress." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/843657.

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We will investigate the effects of exenatide on vascular endothelial injury and nitrooxidative stress in hyperglycemia both in vivo and in vitro and explore the role of nitrooxidative stress in endothelium-protective action of exenatide. Healthy male Wistar rats were randomly divided into 4 groups: control, diabetes mellitus (DM) model, low dose of exenatide treatment, and high dose of exenatide treatment. In vitro study showed that, compared with control group, the DM rats exhibited a lowered endothelium-dependent relaxation and damaged structural integrity of thoracic aortas, and there was a significant increase in plasma nitrotyrosine concentration. These parameters were improved after treatment with either low dose or high dose of exenatide for 45 days. In vitro study showed that exendin-4 (the active ingredient of exenatide) attenuated HUVECs injury induced by high glucose, with improving cell viability and attenuating cell apoptosis. Exendin-4 also significantly alleviated the increased malondialdehyde (MDA), nitrotyrosine content, and inducible nitric oxide synthase (iNOS) expression induced by high glucose in HUVECs. In conclusion, this study demonstrates that exenatide treatment can alleviate the vascular endothelial injury, as well as attenuating the nitrooxidative stress in hyperglycemia, implying that the endothelium-protective effect of exenatide might be related to the reduction of nitrooxidative stress.
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4

McCord, Amie D. "Exenatide: A Novel Therapeutic Approach for Type 2 Diabetes Mellitus." Journal of Pharmacy Technology 21, no. 4 (July 2005): 191–96. http://dx.doi.org/10.1177/875512250502100402.

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Objective: To review the pharmacology, pharmacokinetics, clinical efficacy and safety studies, adverse effects, drug interactions, and dosage and administration of exenatide, a novel incretin mimetic agent recently approved for the treatment of type 2 diabetes mellitus. Data Sources: Information was obtained from MEDLINE searches of the English-language literature (1990–November 2004). Search terms included exenatide, synthetic exendin-4, exendin-4, AC2993, and GLP-1 agonist. Study Selection and Data Extraction: All available data were reviewed, including animal and human data disseminated as abstracts, clinical trials, review articles, and press releases. Data Synthesis: Exenatide is a novel therapeutic agent recently approved for the treatment of type 2 diabetes. The unique pharmacologic profile of exenatide offers a promising adjunctive treatment option for this patient population. Conclusions: While the long-term safety and efficacy of this agent are not well documented, the available data indicate the efficacy and safety of exenatide in combination with various oral antidiabetic agents in reducing postprandial glucose concentrations, glycosylated hemoglobin values, and potentially body weight without increasing the risk of hypoglycemia.
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5

Denker, P. S., and P. E. Dimarco. "Exenatide (Exendin-4)-Induced Pancreatitis: A case report." Diabetes Care 29, no. 2 (January 27, 2006): 471. http://dx.doi.org/10.2337/diacare.29.02.06.dc05-2043.

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6

Kosowska, Agnieszka, Enrique Gallego-Colon, Wojciech Garczorz, Agnieszka Kłych-Ratuszny, Mohammad Reza F. Aghdam, Michał Woz´niak, Andrzej Witek, et al. "Exenatide modulates tumor–endothelial cell interactions in human ovarian cancer cells." Endocrine Connections 6, no. 8 (November 2017): 856–65. http://dx.doi.org/10.1530/ec-17-0294.

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Diabetes and cancer are prevalent diseases whose incidence is increasing globally. Diabetic women have a moderate risk increase in ovarian cancer, suggested to be due to an interaction between these two disorders. Furthermore, patients manifesting both diseases have associated worse prognosis, reduced survival and shorter relapse-free survival. According to current recommendations, incretin drugs such as Exenatide, a synthetic analog of Exendin-4, and Liraglutide are used as therapy for the type 2 diabetes (T2D). We studied the effects of GLP-1 and Exendin-4 on migration, apoptosis and metalloproteinase production in two human ovarian cancer cells (SKOV-3 and CAOV-3). Exendin-4 inhibited migration and promoted apoptosis through caspase 3/7 activation. Exendin-4 also modulated the expression of key metalloproteinases (MMP-2 and MMP-9) and their inhibitors (TIMP-1 and TIMP-2). Vascular endothelial cells, which contribute to the formation and progression of metastasis, were also analyzed. TNF-α-stimulated endothelial cells from iliac artery after Exendin-4 treatment showed reduced production of adhesion molecules (ICAM-1 and VCAM-1). Additionally, incretin treatment inhibited activation of apoptosis in TNF-α-stimulated endothelial cells. In the same experiment, MMPs (MMP-1 and MMP-9), which are relevant for tumor development, were also reduced. Our study demonstrated that incretin drugs may reduce cancer cell proliferation and dissemination potential, hence limiting the risk of metastasis in epithelial ovarian cancer.
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7

Hiles, Richard A., Roger E. Bawdon, and Ezio M. Petrella. "Ex vivo human placental transfer of the peptides pramlintide and exenatide (synthetic exendin-4)." Human & Experimental Toxicology 22, no. 12 (December 2003): 623–28. http://dx.doi.org/10.1191/0960327103ht402oa.

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Two peptides, pramlintide (37 amino acids), an analog of human amylin, and exenatide, synthetic exendin-4 (39 amino acids), are both in late-stage clinical development as potential new treatments for people with diabetes. Both are potential long-term treatments, and there is the likelihood that some women will become pregnant while using one of these peptide therapies. Therefore, it was important to evaluate the potential for each peptide to cross the placental barrier and thereby result in exposure to the fetus. This was examined using ex vivo perfusions of human placentas. The fetal and maternal side of a cotyledon were cannulated and perfused first with buffer, and then with radioactive antipyrine in order to establish the integrity of the system and the perfusion constants. Either pramlintide or exenatide was then added to each acceptable cotyledon perfusate on the maternal side. Each peptide was evaluated at an initial concentration near the therapeutic plasma concentration and at approximately 10-50 times that concentration in each of the three cotyledons. Maternal and fetal perfusate samples were assayed for peptide concentrations using an immunoassay. The ratio of fetal-to-maternal peptide concentrations during equilibrium perfusion were extremely low (pramlintide ≤ 0.006, exenatide 5 ≤ 0.017). These data demonstrate negligible passage of either peptide across the placental barrier. It is, therefore, likely that maternal use of either peptide during gestation will result in negligible exposure to the fetus.
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8

Kawasaki, Yukiko, Yoshiyuki Hamamoto, and Hiroyuki Koshiyama. "Species-Specific Actions of Incretin: From the Evolutionary Perspective." Japanese Clinical Medicine 1 (January 2010): JCM.S5915. http://dx.doi.org/10.4137/jcm.s5915.

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Two modes of incretin-based therapy, incretin mimetics (ie, glucagon-like peptide-1 (GLP-1) agonists) and incretin enhancers (ie, inhibitors of dipeptidyl peptidase IV (DPP-IV)), have recently been introduced into the clinical use. From the viewpoint of evolutionary endocrinology of GLP-1 and their receptors, the incretin action of GLP-1 seems to be relatively recent. Exendin-3 and exendin-4 are paralogs of GLP-1 from the lizards, and the synthetic exendin-4, exenatide, is a paralog of GLP-1. It has recently been indicated that GLP-1 and its receptor are expressed in the taste buds of the tongue, suggesting their possible function in the taste sensing signal pathway. In order to elucidate unknown functions of GLP-1 and its agonists and enhancers, ie, other than incretin actions in humans, it is possibly useful to consider GLP-1 from the viewpoint of integrated systems biology and evolutionary endocrinology.
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9

Nachnani, J. S., D. G. Bulchandani, A. Nookala, B. Herndon, A. Molteni, P. Pandya, R. Taylor, T. Quinn, L. Weide, and L. M. Alba. "Biochemical and histological effects of exendin-4 (exenatide) on the rat pancreas." Diabetologia 53, no. 1 (September 13, 2009): 153–59. http://dx.doi.org/10.1007/s00125-009-1515-4.

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10

Calara, F. "Effect of injection site on relative bioavailability of exenatide (synthetic exendin-4)." Clinical Pharmacology & Therapeutics 75, no. 2 (February 2004): P58. http://dx.doi.org/10.1016/j.clpt.2003.11.221.

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