Expression of Gastrin Family Peptides in Pancreatic Islets and Their Role in β-Cell Function and Survival
| العنوان: | Expression of Gastrin Family Peptides in Pancreatic Islets and Their Role in β-Cell Function and Survival |
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| المؤلفون: | R. Charlotte Moffett, Peter R. Flatt, Nigel Irwin, Srividya Vasu, Dawood Khan |
| المصدر: | Pancreas. 47:190-199 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | Blood Glucose, Male, 0301 basic medicine, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, digestive system, Glucagon, Diabetes Mellitus, Experimental, Islets of Langerhans, 03 medical and health sciences, Endocrinology, Insulin-Secreting Cells, Internal medicine, Gastrins, Insulin Secretion, Internal Medicine, medicine, Animals, Humans, Insulin, Cells, Cultured, Cell Proliferation, Gastrin, Cholecystokinin, Gastrin family, Hepatology, Chemistry, Pancreatic islets, digestive, oral, and skin physiology, Streptozotocin, Peptide Fragments, Mice, Inbred C57BL, Glucose, 030104 developmental biology, medicine.anatomical_structure, Beta cell, Peptides, hormones, hormone substitutes, and hormone antagonists, medicine.drug |
| الوصف: | Objectives Modulation of cholecystokinin (CCK) receptors has been shown to influence pancreatic endocrine function. Methods We assessed the impact of the CCKA and CCKB receptor modulators, (pGlu-Gln)-CCK-8 and gastrin-17, respectively, on β-cell secretory function, proliferation and apoptosis and glucose tolerance, and investigating alterations of CCK and gastrin islet expression in diabetes. Results Initially, the presence of CCK and gastrin, and expression of their receptors were evidenced in β-cell lines and mouse islets. (pGlu-Gln)-CCK-8 and gastrin-17 stimulated insulin secretion from BRIN-BD11 and 1.1B4 β-cells, associated with no effect on membrane potential or [Ca]i. Only (pGlu-Gln)-CCK-8 possessed insulin secretory actions in isolated islets. In agreement, (pGlu-Gln)-CCK-8 improved glucose disposal and glucose-induced insulin release in mice. In addition, (pGlu-Gln)-CCK-8 evoked clear satiety effects. Interestingly, islet colocalization of CCK with glucagon was elevated in streptozotocin- and hydrocortisone-induced diabetic mice, whereas gastrin coexpression in α cells was reduced. In contrast, gastrin colocalization within β-cells was higher in diabetic mice, while CCK coexpression with insulin was decreased in insulin-deficient mice. (pGlu-Gln)-CCK-8 and gastrin-17 also augmented human and rodent β-cell proliferation and offered protection against streptozotocin-induced β-cell cytotoxicity. Conclusions We highlight the direct involvement of CCKA and CCKB receptors in pancreatic β-cell function and survival. |
| تدمد: | 1536-4828 0885-3177 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::51fa925515c414f9d0750b641fcf1696Test https://doi.org/10.1097/mpa.0000000000000983Test |
| رقم الانضمام: | edsair.doi.dedup.....51fa925515c414f9d0750b641fcf1696 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15364828 08853177 |
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