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Pancreatic islet

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https://www.readbyqxmd.com/read/29145151/vildagliptin-loaded-triangular-dna-nanospheres-coated-with-eudragit-for-oral-delivery-and-better-glycemic-control-in-type-2-diabetes-mellitus
#1
Mirza Muhammad Faran Ashraf Baig, Sara Khan, Muhammad Ahsan Naeem, Ghulam Jilany Khan, Muhammad Tayyab Ansari
Diabetes mellitus type 2 is a multidimensional disease associated with poor glycemic control through compromised sensitivity of pancreatic islet α and β cells against glucose and dwindled secretion of insulin which is linked with the quantity of incretin hormones that are abridged by dipeptidyl peptidase-4 (DPP-4) in diseased condition. Vildagliptin (VG) inhibits DPP-4 therefore regulates the incretins that conversely maintains glycemic control. The safe reach and absorption of VG from intestine was dubious...
November 13, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29145016/thermal-effect-on-the-degradation-of-hiapp20-29-fibrils
#2
H X Zhang, Lei Liu, Jie Wang, Christian Bortolini, Mingdong Dong
Uncontrolled misfolding of proteins resulting in the formation of amyloid deposits is associated with over 40 types of diseases, for instance, type-2 diabetes. The human Islet amyloid polypeptide (hIAPP) amyloid formation is thought to be the cause of type-2 diabetes occurrence. A possible strategy to the current challenge of reducing the toxicity of its aggregates to pancreatic β-cell is the discovery of an efficient way to degrading amyloid deposits. In this work, hIAPP20-29, a core fibrillating fragment of hIAPP, was selected as model system to explore the thermal effect at different temperature on the degradation of hIAPP20-29 mature fibrils...
October 31, 2017: Journal of Colloid and Interface Science
https://www.readbyqxmd.com/read/29142323/nkx6-1-decline-accompanies-mitochondrial-dna-reduction-but-subtle-nucleoid-size-decrease-in-pancreatic-islet-%C3%AE-cells-of-diabetic-goto-kakizaki-rats
#3
Tomáš Špaček, Vojtěch Pavluch, Lukáš Alán, Nikola Capková, Hana Engstová, Andrea Dlasková, Zuzana Berková, František Saudek, Petr Ježek
Hypertrophic pancreatic islets (PI) of Goto Kakizaki (GK) diabetic rats contain a lower number of β-cells vs. non-diabetic Wistar rat PI. Remaining β-cells contain reduced mitochondrial (mt) DNA per nucleus (copy number), probably due to declining mtDNA replication machinery, decreased mt biogenesis or enhanced mitophagy. We confirmed mtDNA copy number decrease down to <30% in PI of one-year-old GK rats. Studying relations to mt nucleoids sizes, we employed 3D superresolution fluorescent photoactivable localization microscopy (FPALM) with lentivirally transduced Eos conjugate of mt single-stranded-DNA-binding protein (mtSSB) or transcription factor TFAM; or by 3D immunocytochemistry...
November 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29138225/androgen-signaling-expands-%C3%AE-cell-mass-in-male-rats-and-%C3%AE-cell-androgen-receptor-is-degraded-under-high-glucose-conditions
#4
Naoki Harada, Yasuhiro Yoda, Yusuke Yotsumoto, Tatsuya Masuda, Yuji Takahashi, Takahiro Katsuki, Kenji Kai, Nobuaki Shiraki, Hiroshi Inui, Ryoichi Yamaji
A deficient pancreatic β-cell mass increases the risk of type 2 diabetes mellitus. Here, we investigated the effects of testosterone on the development of pancreatic β-cell mass in male rats. The β-cell mass of male rats castrated at 6 weeks of age was reduced to ~30% of that of control rats at 16 weeks of age, and castration caused glucose intolerance. Loss of β-cell mass occurred due to decreases in islet density/pancreas and β-cell cluster size. Castration was negatively associated with the number of Ki67-positive β-cells and positively associated with the number of TUNEL-positive β-cells...
November 14, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/29135679/characterization-of-the-human-pancreas-side-population-as-a-potential-reservoir-of-adult-stem-cells
#5
Petra Augstein, Thomas Loudovaris, Esther Bandala-Sanchez, Peter Heinke, Gaetano Naselli, Lily Lee, Wayne J Hawthorne, L Jorge Góñez, Alana M Neale, François Vaillant, Helen E Thomas, Thomas W Kay, Ilia Banakh, Leonard C Harrison
OBJECTIVES: The side population (SP) contains cells with stem cell/progenitor properties. Previously, we observed that the mouse pancreas SP expanded after pancreatic injury. We aimed to characterize the SP in human pancreas as a potential source of stem cells. METHODS: Human organ donor pancreata were fractionated into islets and exocrine tissue, enriched by tissue culture and dispersed into single cells. Cells were phenotyped by flow cytometry, and the SP was defined by efflux of fluorescent dye Hoechst 33342 visualized by ultraviolet excitation...
November 10, 2017: Pancreas
https://www.readbyqxmd.com/read/29134966/total-pancreatectomy-and-islet-autotransplant-in-the-treatment-of-chronic-pancreatitis-tread-very-very-carefully
#6
Timothy B Gardner, Kerrington D Smith
No abstract text is available yet for this article.
November 14, 2017: American Journal of Gastroenterology
https://www.readbyqxmd.com/read/29133483/ctage5-deletion-in-pancreatic-%C3%AE-cells-impairs-proinsulin-trafficking-and-insulin-biogenesis-in-mice
#7
Junwan Fan, Yaqing Wang, Liang Liu, Hongsheng Zhang, Feng Zhang, Lei Shi, Mei Yu, Fei Gao, Zhiheng Xu
Proinsulin is synthesized in the endoplasmic reticulum (ER) in pancreatic β cells and transported to the Golgi apparatus for proper processing and secretion into plasma. Defects in insulin biogenesis may cause diabetes. However, the underlying mechanisms for proinsulin transport are still not fully understood. We show that β cell-specific deletion of cTAGE5, also known as Mea6, leads to increased ER stress, reduced insulin biogenesis in the pancreas, and severe glucose intolerance in mice. We reveal that cTAGE5/MEA6 interacts with vesicle membrane soluble N-ethyl-maleimide sensitive factor attachment protein receptor Sec22b...
November 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/29133420/resident-macrophages-of-pancreatic-islets-have-a-seminal-role-in-the-initiation-of-autoimmune-diabetes-of-nod-mice
#8
Javier A Carrero, Derrick P McCarthy, Stephen T Ferris, Xiaoxiao Wan, Hao Hu, Bernd H Zinselmeyer, Anthony N Vomund, Emil R Unanue
Treatment of C57BL/6 or NOD mice with a monoclonal antibody to the CSF-1 receptor resulted in depletion of the resident macrophages of pancreatic islets of Langerhans that lasted for several weeks. Depletion of macrophages in C57BL/6 mice did not affect multiple parameters of islet function, including glucose response, insulin content, and transcriptional profile. In NOD mice depleted of islet-resident macrophages starting at 3 wk of age, several changes occurred: (i) the early entrance of CD4 T cells and dendritic cells into pancreatic islets was reduced, (ii) presentation of insulin epitopes by dispersed islet cells to T cells was impaired, and (iii) the development of autoimmune diabetes was significantly reduced...
November 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29133412/cell-autonomous-adiposity-through-increased-cell-surface-glut4-due-to-ankyrin-b-deficiency
#9
Damaris N Lorenzo, Vann Bennett
Obesity typically is linked to caloric imbalance as a result of overnutrition. Here we propose a cell-autonomous mechanism for adiposity as a result of persistent cell surface glucose transporter type 4 (GLUT4) in adipocytes resulting from impaired function of ankyrin-B (AnkB) in coupling GLUT4 to clathrin-mediated endocytosis. Adipose tissue-specific AnkB-KO mice develop obesity and progressive pancreatic islet dysfunction with age or high-fat diet (HFD). AnkB-deficient adipocytes exhibit increased lipid accumulation associated with increased glucose uptake and impaired endocytosis of GLUT4...
November 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29132171/metabolic-endotoxemia-activated-macrophages-promote-pancreatic-%C3%AE-cell-death-via-ifn%C3%AE-xaf1-pathway
#10
Mitsudai Tsuruta, Misaki Iwashita, Takanori Shinjo, Hiroaki Matsunaga, Akiko Yamashita, Fusanori Nishimura
Metabolic endotoxemia has been implicated in the pathogenesis of type 2 diabetes. In addition to adipose tissue inflammation, inflammatory cell infiltration is also observed in islets, although its effect on islets is largely unknown. We hypothesized that macrophage infiltration into islets leads to impairment of α or β cell function, which ultimately act to exacerbate the pathophysiology of diabetes. Gene expression in a murine α cell line, αTC1, and β cell line, βTC6, was investigated by DNA microarray after co-culturing the cells with a murine macrophage cell line, RAW 264...
November 13, 2017: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
https://www.readbyqxmd.com/read/29132136/meg3-suppresses-human-pancreatic-neuroendocrine-tumor-cells-growth-and-metastasis-by-down-regulation-of-mir-183
#11
Yuan-Yuan Zhang, Hao-Miao Feng
BACKGROUND/AIMS: Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms which arise from pancreatic islet cells. Recently, lncRNA MEG3 has been reported as a tumor suppressor in variety cancers. This study aimed to reveal the functional effects of MEG3 on pNETs which has not been uncovered previously. METHODS: The expression of MEG3, miR-183, and BRI3 in BON1 cells were altered by transfection with their specific vectors/shRNA, or mimic/inhibitor. Thereafter, cell viability, apoptosis, the protein expressions of cell cycle related factors, and apoptosis associated factors, as well as cell migration and invasion were respectively assessed by typan blue staining, flow cytometry, western blotting, and transwell assay...
November 13, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29131920/congenital-hyperinsulinism
#12
Elena Minakova, Alison Chu
Congenital hyperinsulinism is a rare disorder that commonly presents in the immediate postnatal period as persistent hypoglycemia. The condition is frequently resistant to medical therapies, and the genetic mutations implicated in the disorder can be predictive of response to therapy. Evaluation of hypoglycemia in the illustrative case presented in this article led to genetic testing identifying recessive mutations in the potassium channel subunits of the beta-islet pancreatic cells. Potassium channel defects are often refractory to medical therapies, so near-total pancreatectomy is usually indicated; however, genetic mutations leading to metabolic dysregulation within the beta-islet pancreatic cells are usually responsive to medical therapy...
November 1, 2017: Pediatric Annals
https://www.readbyqxmd.com/read/29128846/tissue-adhesive-fk506-loaded-polymeric-nanoparticles-for-multi-layered-nano-shielding-of-pancreatic-islets-to-enhance-xenograft-survival-in-a-diabetic-mouse-model
#13
Tung Thanh Pham, Tiep Tien Nguyen, Shiva Pathak, Shobha Regmi, Hanh Thuy Nguyen, Tuan Hiep Tran, Chul Soon Yong, Jong Oh Kim, Pil-Hoon Park, Min Hui Park, Young Kyung Bae, Jeong Uk Choi, Youngro Byun, Cheol-Hee Ahn, Simmyung Yook, Jee-Heon Jeong
This study aims to develop a novel surface modification technology to prolong the survival time of pancreatic islets in a xenogenic transplantation model, using 3,4-dihydroxyphenethylamine (DOPA) conjugated poly(lactide-co-glycolide)-poly(ethylene glycol) (PLGA-PEG) nanoparticles (DOPA-NPs) carrying immunosuppressant FK506 (FK506/DOPA-NPs). The functionalized DOPA-NPs formed a versatile coating layer for antigen camouflage without interfering the viability and functionality of islets. The coating layer effectively preserved the morphology and viability of islets in a co-culture condition with xenogenic lymphocytes for 7 days...
November 1, 2017: Biomaterials
https://www.readbyqxmd.com/read/29128354/angiotensin-converting-enzyme-2-regulates-mitochondrial-function-in-pancreatic-%C3%AE-cells
#14
Ting-Ting Shi, Fang-Yuan Yang, Chang Liu, Xi Cao, Jing Lu, Xue-Lian Zhang, Ming-Xia Yuan, Chen Chen, Jin-Kui Yang
Mitochondrial metabolism plays an essential role in the regulation of insulin release and glucose homeostasis. Evidence demonstrated that the angiotensin-converting enzyme 2 (ACE2) participates in the regulation of glucose metabolism, however, its role in mitochondrial metabolism remains unclear. The purpose of our study was to determine if ACE2 can regulate mitochondrial function in pancreatic β-cells. We found that ACE2 over-expression restored glucose-stimulated insulin secretion (GSIS) and mitochondrial membrane potential (MMP) in the presence of H2O2 in INS-1 cells...
November 8, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29123178/a-nanobody-based-tracer-targeting-dpp6-for-non-invasive-imaging-of-human-pancreatic-endocrine-cells
#15
Alexander Balhuizen, Sam Massa, Iris Mathijs, Jean-Valery Turatsinze, Jens De Vos, Stéphane Demine, Catarina Xavier, Olatz Villate, Isabelle Millard, Dominique Egrise, Carmen Capito, Raphaël Scharfmann, Pieter In't Veld, Piero Marchetti, Serge Muyldermans, Serge Goldman, Tony Lahoutte, Luc Bouwens, Decio L Eizirik, Nick Devoogdt
There are presently no reliable ways to quantify endocrine cell mass (ECM) in vivo, which prevents an accurate understanding of the progressive beta cell loss in diabetes or following islet transplantation. To address this unmet need, we coupled RNA sequencing of human pancreatic islets to a systems biology approach to identify new biomarkers of the endocrine pancreas. Dipeptidyl-Peptidase 6 (DPP6) was identified as a target whose mRNA expression is at least 25-fold higher in human pancreatic islets as compared to surrounding tissues and is not changed by proinflammatory cytokines...
November 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29122960/mir-335-overexpression-impairs-insulin-secretion-through-defective-priming-of-insulin-vesicles
#16
Vishal A Salunkhe, Jones K Ofori, Nikhil R Gandasi, Sofia A Salö, Sofia Hansson, Markus E Andersson, Anna Wendt, Sebastian Barg, Jonathan L S Esguerra, Lena Eliasson
MicroRNAs contribute to the maintenance of optimal cellular functions by fine-tuning protein expression levels. In the pancreatic β-cells, imbalances in the exocytotic machinery components lead to impaired insulin secretion and type 2 diabetes (T2D). We hypothesize that dysregulated miRNA expression exacerbates β-cell dysfunction, and have earlier shown that islets from the diabetic GK-rat model have increased expression of miRNAs, including miR-335-5p (miR-335). Here, we aim to determine the specific role of miR-335 during development of T2D, and the influence of this miRNA on glucose-stimulated insulin secretion and Ca(2+)-dependent exocytosis...
November 2017: Physiological Reports
https://www.readbyqxmd.com/read/29121068/metabolic-regulation-of-glp-1-and-pc1-3-in-pancreatic-%C3%AE-cell-line
#17
Veronica Sancho, Giuseppe Daniele, Daniela Lucchesi, Roberto Lupi, Annamaria Ciccarone, Giuseppe Penno, Cristina Bianchi, Angela Dardano, Roberto Miccoli, Stefano Del Prato
BACKGROUND AND AIMS: An intra-islet incretin system has been recently suggested to operate through modulation of the expression and activity of proconvertase 1/3 and 2 (PC1/3, PC2) in pancreatic alpha-cell accounting for local release of GLP-1. Little is known, whether this alpha-cell activity can be affected by the metabolic alterations occurring in type 2 diabetes, such as hyperglycemia, hyperlipidemia or hyperglucagonemia. MATERIALS AND METHODS: AlphaTC1/6 cells from a mice pancreatic cell line were incubated in the presence of two glucose (G) concentration (5...
2017: PloS One
https://www.readbyqxmd.com/read/29119245/development-and-characterisation-of-a-novel-glucagon-like-peptide-1-receptor-antibody
#18
Emma K Biggs, Lihuan Liang, Jacqueline Naylor, Shimona Madalli, Rachel Collier, Matthew P Coghlan, David J Baker, David C Hornigold, Peter Ravn, Frank Reimann, Fiona M Gribble
AIMS/HYPOTHESIS: Glucagon like peptide-1 (GLP-1) enhances glucose-dependent insulin secretion by binding to GLP-1 receptors (GLP1Rs) on pancreatic beta cells. GLP-1 mimetics are used in the clinic for the treatment of type 2 diabetes, but despite their therapeutic success, several clinical effects of GLP-1 remain unexplained at a mechanistic level, particularly in extrapancreatic tissues. The aim of this study was to generate and characterise a monoclonal antagonistic antibody for the GLP1R for use in vivo...
November 9, 2017: Diabetologia
https://www.readbyqxmd.com/read/29118817/maternal-high-fat-diet-impairs-glucose-metabolism-%C3%AE-cell-function-and-proliferation-in-the-second-generation-of-offspring-rats
#19
Yan-Hong Huang, Ting-Ting Ye, Chong-Xiao Liu, Lei Wang, Yuan-Wen Chen, Yan Dong
Background: This study aimed to assess the impact of perinatal high-fat (HF) diet in female Sprague-Dawley rats (F0) on glucose metabolism and islet function in their early life of second-generation of offspring (F2). Methods: F0 rats were fed with a standard chow (SC) or HF diet for 8 weeks before mating, up to termination of lactation for their first-generation of offspring (F1-SC and F1-HF). F1 females were mated with normal males at the age of week 11, and producing F2 offspring (F2-SC, F2-HF)...
2017: Nutrition & Metabolism
https://www.readbyqxmd.com/read/29118086/creb-crtc2-controls-glp-1-dependent-regulation-of-glucose-homeostasis
#20
Ji-Hyun Lee, Xianlan Wen, Hana Cho, Seung-Hoi Koo
Glucagon-like peptide 1 (GLP-1) is a major incretin that controls glucose homeostasis. The secretion of mature GLP-1 is regulated via GPCRs, including bile acid receptor G protein-coupled bile acid receptor 1, which uses cAMP signaling to enhance the exocytosis of GLP-1-containing vesicles. However, the role of cAMP-mediated transcription has not been clearly demonstrated to date. In this study, we explored the role of cAMP response element-binding protein/CREB-regulated transcription coactivator 2 (CREB/CRTC2)-dependent transcription on GLP-1 secretion in the L cells...
November 8, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
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