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https://www.readbyqxmd.com/read/27920090/islet-derived-cd4-t-cells-targeting-proinsulin-in-human-autoimmune-diabetes
#1
Aaron W Michels, Laurie G Landry, Kristen A McDaniel, Liping Yu, Martha Campbell-Thompson, William W Kwok, Kenneth L Jones, Peter A Gottlieb, John W Kappler, Qizhi Tang, Bart O Roep, Mark A Atkinson, Clayton E Mathews, Maki Nakayama
Type 1 diabetes results from chronic autoimmune destruction of insulin-producing beta cells within pancreatic islets. While insulin is a critical self-antigen in animal models of autoimmune diabetes, due to extremely limited access to pancreas samples, little is known about human antigenic targets for islet-infiltrating T-cells. Here we show that proinsulin peptides are targeted by islet-infiltrating T-cells from type 1 diabetes patients. We identified hundreds of T-cells from inflamed pancreatic islets of three young type 1 diabetes organ donors with a short disease duration with high risk HLA genes using a direct T-cell receptor (TCR) sequencing approach without long-term cell culture...
December 5, 2016: Diabetes
https://www.readbyqxmd.com/read/27919855/uncoupling-protein-2-deficiency-reduces-proliferative-capacity-of-murine-pancreatic-stellate-cells
#2
Sarah Muller, Sandra Maria Klingbeil, Andreea Sandica, Robert Jaster
BACKGROUND: Uncoupling protein 2 (UCP2) has been suggested to inhibit mitochondrial production of reactive oxygen species (ROS) by decreasing the mitochondrial membrane potential. Experimental acute pancreatitis is associated with increased UCP2 expression, whereas UCP2 deficiency retards regeneration of aged mice from acute pancreatitis. Here, we have addressed biological and molecular functions of UCP2 in pancreatic stellate cells (PSCs), which are involved in pancreatic wound repair and fibrogenesis...
December 2016: Hepatobiliary & Pancreatic Diseases International: HBPD INT
https://www.readbyqxmd.com/read/27914538/adaptive-response-of-rat-pancreatic-%C3%AE-cells-to-insulin-resistance-induced-by-monocrotophos-biochemical-evidence
#3
Raju Nagaraju, Padmanabhan Sharda Rajini
Our previous findings clearly suggested the role of duration of exposure to monocrotophos (MCP) in the development of insulin resistance. Rats exposed chronically to MCP developed insulin resistance with hyperinsulinemia without overt diabetes. In continuation of this vital observation, we sought to delineate the biochemical mechanisms that mediate heightened pancreatic β-cell response in the wake of MCP-induced insulin resistance in rats. Adult rats were orally administered (0.9 and 1.8mg/kgb.w/d) MCP for 180days...
November 2016: Pesticide Biochemistry and Physiology
https://www.readbyqxmd.com/read/27912197/rac1-nadph-oxidase-signaling-promotes-cd36-activation-under-glucotoxic-conditions-in-pancreatic-beta-cells
#4
Suma Elumalai, Udayakumar Karunakaran, In Kyu Lee, Jun Sung Moon, Kyu Chang Won
We recently reported that cluster determinant 36 (CD36), a fatty acid transporter, plays a pivotal role in glucotoxicity-induced β-cell dysfunction. However, little is known about how glucotoxicity influences CD36 expression. Emerging evidence suggests that the small GTPase Rac1 is involved in the pathogenesis of beta cell dysfunction in type 2 diabetes (T2D). The primary objective of the current study was to determine the role of Rac1 in CD36 activation and its impact on β-cell dysfunction in diabetes mellitus...
November 23, 2016: Redox Biology
https://www.readbyqxmd.com/read/27910859/t-cell-programming-in-pancreatic-adenocarcinoma-a-review
#5
REVIEW
Y D Seo, V G Pillarisetty
Despite recent advancements in multimodal therapy, pancreatic ductal adenocarcinoma (PDA) continues to have a dismal prognosis. In the era of burgeoning immune therapies against previously difficult-to-treat malignancies, there has been growing interest in activating the immune system against PDA; however, unlike in other cancers such as melanoma and lymphoma, immunotherapy has not yielded many clinically significant results. To harness these mechanisms for therapeutic use, an in-depth understanding of T-cell programming in the immune microenvironment of PDA must be achieved...
December 2, 2016: Cancer Gene Therapy
https://www.readbyqxmd.com/read/27910284/resting-heart-rate-is-an-independent-predictor-of-death-in-patients-with-colorectal-pancreatic-and-non-small-cell-lung-cancer-results-of-a-prospective-cardiovascular-long-term-study
#6
Markus S Anker, Nicole Ebner, Bert Hildebrandt, Jochen Springer, Marianne Sinn, Hanno Riess, Stefan D Anker, Ulf Landmesser, Wilhelm Haverkamp, Stephan von Haehling
AIMS: Patients with advanced cancer have been shown to suffer from abnormal cardiac function and impaired exercise capacity that may contribute to their impaired quality of life. As tachycardia is considered as a sign of potential early cardiac damage, we sought to determine whether resting heart rate and other ECG-derived variables have prognostic value. METHODS AND RESULTS: From 2005 to 2010, we enrolled 145 patients with histologically confirmed cancer (36 colorectal, 72 pancreatic, and 37 non-small cell lung cancer patients) and 59 healthy controls...
December 2016: European Journal of Heart Failure
https://www.readbyqxmd.com/read/27909574/characterization-of-5-2-18-f-fluoroethoxy-l-tryptophan-for-pet-imaging-of-the-pancreas
#7
Ahmed Abbas, Christine Beamish, Rebecca McGirr, John Demarco, Neil Cockburn, Dawid Krokowski, Ting-Yim Lee, Michael Kovacs, Maria Hatzoglou, Savita Dhanvantari
Purpose: In diabetes, pancreatic beta cell mass declines significantly prior to onset of fasting hyperglycemia. This decline may be due to endoplasmic reticulum (ER) stress, and the system L amino acid transporter LAT1 may be a biomarker of this process. In this study, we used 5-(2- (18)F-fluoroethoxy)-L-tryptophan ( (18)F-L-FEHTP) to target LAT1 as a potential biomarker of beta cell function in diabetes. Procedures: Uptake of (18)F-L-FEHTP was determined in wild-type C57BL/6 mice by ex vivo biodistribution...
2016: F1000Research
https://www.readbyqxmd.com/read/27903221/in-vitro-generated-mesenchymal-stem-cells-suitable-tools-to-target-insulin-dependent-diabetes-mellitus
#8
Shruti D Dave, Patel C N, Patel J V, Thakkar U G
A synergy of a pre-accumulated genes with an autoimmunity advancing to slow abolition of pancreatic beta-cells causes insulin deficiency and results enrooting insulin dependent diabetes mellitus (IDDM). As per WHO data worldwide about 150 million people are diabetic and the number may rise to more than double by the year 2025. Any absolute cure for IDDM is not available yet, and one of the credible advent in the field include cell-based therapy. At this conjecture, mesenchymal stem cells (MSC) seems to have a specific and beneficial characteristics due to their in vivo as well as in vitro potential to mimic a pancreatic endocrine phenotype and immune-regulatory actions...
November 21, 2016: Current Stem Cell Research & Therapy
https://www.readbyqxmd.com/read/27900263/islet-chrebp-%C3%AE-is-increased-in-diabetes-and-controls-chrebp-%C3%AE-and-glucose-induced-gene-expression-via-a-negative-feedback-loop
#9
Gu Jing, Junqin Chen, Guanlan Xu, Anath Shalev
OBJECTIVE: Carbohydrate-response element-binding protein (ChREBP) is the major transcription factor conferring glucose-induced gene expression in pancreatic islets, liver and adipose tissue. Recently, a novel ChREBP isoform, ChREBP-β, was identified in adipose tissue and found to be also expressed in islets and involved in glucose-induced beta cell proliferation. However, the physiological function of this less abundant β-isoform in the islet, and in diabetes, is largely unknown. The aims of the present study, therefore, were to determine how diabetes affects ChREBP-β and elucidate its physiological role in pancreatic beta cells...
December 2016: Molecular Metabolism
https://www.readbyqxmd.com/read/27899481/hznt8-slc30a8-transgenic-mice-which-overexpress-the-r325w-polymorph-have-reduced-islet-zn2-and-proinsulin-levels-increased-glucose-tolerance-after-a-high-fat-diet-and-altered-levels-of-pancreatic-zinc-binding-proteins
#10
Li Li, Shi Bai, Christian T Sheline
Zinc is involved in both type-1 (T1DM) and type-2 (T2DM) diabetes. The wildtype (WT) form of the beta-cell specific Zn(2+) transporter, ZNT8, is linked to T2DM susceptibility. ZnT8 null mice have a mild phenotype with a slight decrease in glucose tolerance, whereas patients with the ZnT8 R325W polymorphism (rs13266634) have decreased proinsulin staining and susceptibility to T2DM. We measured zinc, insulin, and proinsulin stainings, and IPGTT in transgenic mice overexpressing hZnT8 WT or hZnT8 R325W fed a normal or high fat diet (HFD)...
November 29, 2016: Diabetes
https://www.readbyqxmd.com/read/27895310/tgf%C3%AE-1-overexpression-is-associated-with-improved-survival-and-low-tumor-cell-proliferation-in-patients-with-early-stage-pancreatic-ductal-adenocarcinoma
#11
Evan S Glazer, Eric Welsh, Jose M Pimiento, Jamie K Teer, Mokenge P Malafa
The role of transforming growth factor beta-type-1 (TGFβ1) in pancreatic ductal adenocarcinoma (PDAC) progression is stage-dependent. We hypothesized that TGFβ1 expression is associated with survival and proliferation markers in patients with early-stage PDAC. We acquired clinicopathologic, treatment, and mRNA expression data from The Cancer Genome Atlas data set for 106 patients identified with stage I/II PDAC who underwent pancreaticoduodenectomy. Patients were categorized as high expression when mRNA expression was ≥75th percentile for each gene...
November 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/27875315/lipid-tuned-zinc-transport-activity-of-human-znt8-correlates-with-risk-for-type-2-diabetes
#12
Chengfeng Merriman, Qiong Huang, Guy A Rutter, Dax Fu
Zinc is a critical element for insulin storage in the secretory granules of pancreatic beta cells. The islet-specific zinc transporter ZnT8 mediates granular sequestration of zinc ions. A genetic variant of human ZnT8 arising from a single nonsynonymous nucleotide change contributes to increased susceptibility to type-2 diabetes (T2D), but it remains unclear how the high-risk variant (R325), which is also a higher-frequency (>50%) allele, is correlated with zinc transport activity. Here, we compared the activity of R325 with that of a low-risk ZnT8 variant (W325)...
November 8, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27874076/oligofructose-as-an-adjunct-in-treatment-of-diabetes-in-nod-mice
#13
Clement Chan, Colin M Hyslop, Vipul Shrivastava, Andrea Ochoa, Raylene A Reimer, Carol Huang
In type 1 diabetes, restoration of normoglycemia can be achieved if the autoimmune attack on beta cells ceases and insulin requirement is met by the residual beta cells. We hypothesize that an adjunctive therapy that reduces insulin demand by increasing insulin sensitivity will improve the efficacy of an immunotherapy in reversing diabetes. We tested the gut microbiota-modulating prebiotic, oligofructose (OFS), as the adjunctive therapy. We treated non-obese diabetic mice with an immunotherapy, monoclonal anti-CD3 antibody (aCD3), with or without concurrent dietary supplement of OFS...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27872147/primary-human-and-rat-beta-cells-release-the-intracellular-autoantigens-gad65-ia-2-and-proinsulin-in-exosomes-together-with-cytokine-induced-enhancers-of-immunity
#14
Chiara Cianciaruso, Edward A Phelps, Miriella Pasquier, Romain Hamelin, Davide Demurtas, Mohamed Alibashe Ahmed, Lorenzo Piemonti, Sachiko Hirosue, Melody A Swartz, Michele De Palma, Jeffrey A Hubbell, Steinunn Baekkeskov
The target autoantigens in several organ-specific autoimmune diseases, including type 1 diabetes (T1D), are intracellular membrane proteins, whose initial encounter with the immune system is poorly understood. Here we propose a new model for how these proteins can initiate autoimmunity. We found that rat and human pancreatic islets release the intracellular β-cell autoantigens in human T1D, GAD65, IA-2 and proinsulin, in exosomes, which are taken up by and activate dendritic cells. Accordingly, anchoring of GAD65 to exosome-mimetic liposomes strongly boosted antigen presentation and T cell activation in the context of the human type 1 diabetes susceptibility haplotype HLA-DR4...
November 21, 2016: Diabetes
https://www.readbyqxmd.com/read/27872144/cytotoxic-1-deoxysphingolipids-are-metabolized-by-a-cytochrome-p450-dependent-pathway
#15
Irina Alecu, Alaa Othman, Anke Penno, Essa M Saied, Christoph Arenz, Arnold von Eckardstein, Thorsten Hornemann
1-Deoxysphingolipids (1-deoxySLs) are atypical sphingolipids which are formed when serine palmitoyltransferase condenses palmitoyl-CoA with alanine instead of serine during sphingolipid synthesis. 1-DeoxySLs are toxic to neurons and pancreatic beta-cells. Pathologically elevated 1-deoxySLs cause the inherited neuropathy HSAN1 and are also found in type 2 diabetes. Diabetic sensory polyneuropathy and HSAN1 are clinically very similar, suggesting that 1-deoxySLs may be implicated in both pathologies. 1-DeoxySLs are considered to be dead-end metabolites, as they lack the C1-hydroxyl group which is essential for the canonical degradation of sphingolipids...
November 21, 2016: Journal of Lipid Research
https://www.readbyqxmd.com/read/27867203/epac2a-null-mice-exhibit-obesity-prone-nature-more-susceptible-to-leptin-resistance
#16
M Hwang, Y Go, J-H Park, S-K Shin, S E Song, B-C Oh, S-S Im, I Hwang, Y H Jeon, I-K Lee, S Seino, D-K Song
BACKGROUND: The exchange protein directly activated by cAMP (Epac), which is primarily involved in cAMP signaling, has been known to be essential for controlling body energy metabolism. Epac has two isoforms: Epac1 and Epac2. The function of Epac1 on obesity was unveiled using Epac1 knockout (KO) mice. However, the role of Epac2 in obesity remains unclear. METHODS: To evaluate the role of Epac2 in obesity, we used Epac2a KO mice, which is dominantly expressed in neurons and endocrine tissues...
November 21, 2016: International Journal of Obesity: Journal of the International Association for the Study of Obesity
https://www.readbyqxmd.com/read/27866701/place-of-sodium-glucose-cotransporter-2-inhibitors-in-east-asian-subjects-with-type-2-diabetes-mellitus-insights-into-the-management-of-asian-phenotype
#17
REVIEW
Lee Ling Lim, Alexander Tong Boon Tan, Kevin Moses, Viraj Rajadhyaksha, Siew Pheng Chan
The burden of type 2 diabetes (T2DM) in East Asia is alarming. Rapid modernization and urbanization have led to major lifestyle changes and a tremendous increase in the prevalence of obesity, metabolic syndrome, and diabetes mellitus. The development of T2DM at a younger age, with lower body mass index, higher visceral adiposity, and more significant pancreatic beta-cell dysfunction compared to Caucasians are factors responsible for the increased prevalence of T2DM in East Asians. Sodium-glucose Cotransporter-2 (SGLT2) inhibitors (canagliflozin, dapaglifozin, empagliflozin, etc...
October 15, 2016: Journal of Diabetes and its Complications
https://www.readbyqxmd.com/read/27865809/duodenal-jejunal-bypass-attenuates-progressive-failure-of-pancreatic-islets-in-streptozotocin-induced-diabetic-rats
#18
Tingfeng Wang, Peng Zhang, Xiong Zhang, Ting Cao, Chengzhu Zheng, Bo Yu
BACKGROUND: Preservation of pancreatic beta cell function has been increasingly appealing in the treatment of type 2 diabetes. Evidence is still limited on how bariatric surgery affects pancreatic beta cell apoptosis. SETTING: University medical center. OBJECTIVE: The study aimed to investigate the effect of a major component of Roux-en-Y gastric bypass, duodenal-jejunal bypass, on protecting pancreatic beta cells from progressive loss. METHODS: Forty-five normal Sprague-Dawley rats were randomly assigned into 3 groups: duodenal-jejunal bypass (DJB) group (n = 16) and sham (S) group (n = 17), based upon the procedure received, and a control (C) group (n = 12) without any procedure performed, to eliminate potential traumatic effects from surgery...
August 31, 2016: Surgery for Obesity and related Diseases: Official Journal of the American Society for Bariatric Surgery
https://www.readbyqxmd.com/read/27864352/single-cell-transcriptomes-identify-human-islet-cell-signatures-and-reveal-cell-type-specific-expression-changes-in-type-2-diabetes
#19
Nathan Lawlor, Joshy George, Mohan Bolisetty, Romy Kursawe, Lili Sun, Sivakamasundari V, Ina Kycia, Paul Robson, Michael L Stitzel
Blood glucose levels are tightly controlled by the coordinated action of at least four cell types constituting pancreatic islets. Changes in the proportion and/or function of these cells are associated with genetic and molecular pathophysiology of monogenic, type 1, and type 2 diabetes (T2D). Cellular heterogeneity impedes precise understanding of the molecular components of each islet cell type that govern islet dysfunction, particularly the less abundant delta and gamma/pancreatic polypeptide (PP) cells. Here, we report single cell transcriptomes for 638 cells from non-diabetic (ND) and T2D human islet samples...
November 18, 2016: Genome Research
https://www.readbyqxmd.com/read/27864307/pancreatic-beta-cells-express-the-fetal-islet-hormone-gastrin-in-rodent-and-human-diabetes
#20
Tehila Dahan, Oren Ziv, Elad Horwitz, Hai Zemmour, Judith Lavi, Avital Swisa, Gil Leibowitz, Frances M Ashcroft, Peter In't Veld, Benjamin Glaser, Yuval Dor
Beta-cell failure in type 2 diabetes (T2D) was recently proposed to involve dedifferentiation of beta-cells and ectopic expression of other islet hormones, including somatostatin and glucagon. Here we show that gastrin, a stomach hormone typically expressed in the pancreas only during embryogenesis, is expressed in islets of diabetic rodents and humans with T2D. While in mice gastrin is expressed insulin+ cells, in humans with T2D gastrin expression occurs in both insulin+ and somatostatin+ cells. Genetic lineage tracing in mice indicates that gastrin expression is turned on in a subset of differentiated beta-cells following exposure to severe hyperglycemia...
November 18, 2016: Diabetes
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