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Diabetes,Islet pancreatic cell

Amy C Kelly, Kate E Smith, William G Purvis, Catherine G Min, Craig S Weber, Amanda M Cooksey, Craig Hasilo, Steven Paraskevas, Thomas M Suszynski, Bradley P Weegman, Miranda J Anderson, Leticia E Camacho, Robert C Harland, Tom Loudovaris, Jana Jandova, Diana S Molano, Nicholas D Price, Ivan G Georgiev, William E Scott, Derek Manas, James Shaw, Doug O'Gorman, Tatsuya Kin, Fiona M McCarthy, Gregory L Szot, Andrew M Posselt, Peter G Stock, Theodore Karatzas, William J Shapiro, Ronald M Lynch, Sean W Limesand, Klearchos K Papas
BACKGROUND: All human islets used in research and for the clinical treatment of diabetes are subject to ischemic damage during pancreas procurement, preservation, and islet isolation. A major factor influencing islet function is exposure of pancreata to cold ischemia during unavoidable windows of preservation by static cold storage (SCS). Improved preservation methods may prevent this functional deterioration. In the present study, we investigated whether pancreas preservation by gaseous oxygen perfusion (persufflation) better preserved islet function versus SCS...
August 8, 2018: Transplantation
Mengju Liu, Jian Peng, Ningwen Tai, James A Pearson, Changyun Hu, Junhua Guo, Lin Hou, Hongyu Zhao, F Susan Wong, Li Wen
AIMS/HYPOTHESIS: Innate immune effectors interact with the environment to contribute to the pathogenesis of the autoimmune disease, type 1 diabetes. Although recent studies have suggested that innate immune Toll-like receptors (TLRs) are involved in tissue development, little is known about the role of TLRs in tissue development, compared with autoimmunity. We aimed to fill the knowledge gap by investigating the role of TLR9 in the development and function of islet beta cells in type 1 diabetes, using NOD mice...
August 9, 2018: Diabetologia
Andhira Vieira, Bastien Vergoni, Monica Courtney, Noémie Druelle, Elisabet Gjernes, Biljana Hadzic, Fabio Avolio, Tiziana Napolitano, Sergi Navarro Sanz, Ahmed Mansouri, Patrick Collombat
In the context of type 1 diabetes research and the development of insulin-producing β-cell replacement strategies, whether pancreatic ductal cells retain their developmental capability to adopt an endocrine cell identity remains debated, most likely due to the diversity of models employed to induce pancreatic regeneration. In this work, rather than injuring the pancreas, we developed a mouse model allowing the inducible misexpression of the proendocrine gene Neurog3 in ductal cells in vivo. These animals developed a progressive islet hypertrophy attributed to a proportional increase in all endocrine cell populations...
2018: PloS One
Sandra Laban, Jessica S Suwandi, Vincent van Unen, Jos Pool, Joris Wesselius, Thomas Höllt, Nicola Pezzotti, Anna Vilanova, Boudewijn P F Lelieveldt, Bart O Roep
Auto-reactive CD8 T-cells play an important role in the destruction of pancreatic β-cells resulting in type 1 diabetes (T1D). However, the phenotype of these auto-reactive cytolytic CD8 T-cells has not yet been extensively described. We used high-dimensional mass cytometry to phenotype autoantigen- (pre-proinsulin), neoantigen- (insulin-DRIP) and virus- (cytomegalovirus) reactive CD8 T-cells in peripheral blood mononuclear cells (PBMCs) of T1D patients. A panel of 33 monoclonal antibodies was designed to further characterise these cells at the single-cell level...
2018: PloS One
Mahboubeh Daneshpajooh, Lena Eliasson, Karl Bacos, Charlotte Ling
AIMS: It has in recent years been established that epigenetic changes contribute to β-cell dysfunction and type 2 diabetes (T2D). For example, we have showed that the expression of histone deacetylase 7 (HDAC7) is increased in pancreatic islets of individuals with T2D and that increased levels of Hdac7 in β-cells impairs insulin secretion. The HDAC inhibitor MC1568 rescued this secretory impairment, suggesting that inhibitors specific for HDAC7 may be useful clinically in the treatment of T2D...
August 7, 2018: Acta Diabetologica
Rehana Akter, Rebekah L Bower, Andisheh Abedini, Ann Marie Schmidt, Debbie L Hay, Daniel P Raleigh
Islet amyloid formation contributes to β-cell death and dysfunction in type-2 diabetes and to the failure of islet transplants. Amylin (Islet amyloid polypeptide, IAPP), a normally soluble 37 residue polypeptide hormone produced in the pancreatic β-cells, is responsible for amyloid formation in type-2 diabetes. The peptide is deficient in type-1 diabetes. Amylin normally plays an adaptive role in metabolism and the development of non-toxic, non-amyloidogenic, bioactive variants of human amylin are of interest for use as adjuncts to insulin therapy...
August 7, 2018: ACS Chemical Biology
Jiajun Sun, Qicheng Ni, Jing Xie, Min Xu, Jun Zhang, Jie Kuang, Yanqiu Wang, Guang Ning, Qidi Wang
Context: Type 2 diabetes (T2D) and pancreatogenic diabetes are both associated with loss of functional β cell mass. Previous studies have proposed β cell dedifferentiation as a mechanism of islet β cell failure, but its significance in humans is still controversial. Objective: To determine whether β-cell dedifferentiation occurs in human T2D with adequate glucose control and in non-diabetic chronic pancreatitis, we examined pancreatic islets from 9 non-diabetic controls, 10 diabetic patients with well-controlled fasting glycemia and 4 non-diabetic chronic pancreatitis individuals...
August 3, 2018: Journal of Clinical Endocrinology and Metabolism
Yoshimitsu Kiriyama, Hiromi Nochi
Amylin, (or islet amyloid polypeptide; IAPP), a 37-amino acid peptide hormone, is released in response to nutrients, including glucose, lipids or amino acids. Amylin is co-stored and co-secreted with insulin by pancreatic islet β-cells. Amylin inhibits food intake, delays gastric emptying, and decreases blood glucose levels, leading to the reduction of body weight. Therefore, amylin as well as insulin play important roles in controlling the level of blood glucose. However, human amylin aggregates and human amylin oligomers cause membrane disruption, endoplasmic reticulum (ER) stress and mitochondrial damage...
August 6, 2018: Cells
Wencheng Zhang, Li Wang, Xinwen Yu, Aihua Jia, Jie Ming, Qiuhe Ji
Type 2 diabetes mellitus (T2DM) is closely related to islet alpha cell mass and viability. Several types of RFamide-related peptides (RFRPs) are involved in regulating proliferation and function of islet cells. However, current understanding of the role of RFamide-related peptide-3 (RFRP-3) in pancreatic alpha cells is limited. Therefore, we investigated the expression of the RFRP-3 receptor, G protein-coupled receptor 147 (GPR147), in mouse islets and alpha TC1 clone 6 cells, and evaluated the function of RFRP-3 on alpha cells...
August 3, 2018: Peptides
Shahrzad Nojehdehi, Sara Soudi, Ardeshir Hesampour, Shima Rasouli, Masoud Soleimani, Seyed Mahmoud Hashemi
Exosomes derived from adipose tissue-derived mesenchymal stem cells (AD-MSCs) have immunomodulatory effects of T-cell inflammatory response and reduction of clinical symptoms on streptozotocin-induced of the type-1 diabetes mellitus (T1DM). Beside control group and untreated T1DM mice, a group of T1DM mice was treated with intraperitoneal injections of characterized exosomes derived from autologous AD-MSCs. Body weight and blood glucose levels were measured during the procedure. Histopathology and immunohistochemistry were used for evaluation of pancreatic islets using hemotoxylin and eosin (H&E) staining and anti-insulin antibody...
August 3, 2018: Journal of Cellular Biochemistry
Eseoghene Ifie, Mark A Russell, Shalinee Dhayal, Pia Leete, Guido Sebastiani, Laura Nigi, Francesco Dotta, Varpu Marjomäki, Decio L Eizirik, Noel G Morgan, Sarah J Richardson
AIMS/HYPOTHESIS: The Coxsackie and adenovirus receptor (CAR) is a transmembrane cell-adhesion protein that serves as an entry receptor for enteroviruses and may be essential for their ability to infect cells. Since enteroviral infection of beta cells has been implicated as a factor that could contribute to the development of type 1 diabetes, it is often assumed that CAR is displayed on the surface of human beta cells. However, CAR exists as multiple isoforms and it is not known whether all isoforms subserve similar physiological functions...
August 3, 2018: Diabetologia
Rita Sofia Garcia Ribeiro, Conny Gysemans, João Paulo Monteiro Carvalho Mori da Cunha, Bella B Manshian, Daniel Jirak, Jan Kriz, Juan Gallo, Manuel Bañobre-López, Tom Struys, Marcel De Cuyper, Chantal Mathieu, Stefaan J Soenen, Willy Gsell, Uwe Himmelreich
Magnetoliposomes (MLs) were synthesized and tested for longitudinal monitoring of transplanted pancreatic islets using magnetic resonance imaging (MRI) in rat models. The rat insulinoma cell line INS-1E and isolated pancreatic islets from outbred and inbred rats were used to optimize labeling conditions in vitro. Strong MRI contrast was generated by islets exposed to 50 µg Fe/ml for 24 hours without any increased cell death, loss of function or other signs of toxicity. In vivo experiments showed that pancreatic islets (50-1000 units) labeled with MLs were detectable for up to 6 weeks post-transplantation in the kidney subcapsular space...
July 31, 2018: Scientific Reports
Sarah J Richardson, Noel G Morgan
The development of islet autoimmunity and type 1 diabetes has long been linked with enteroviral infection but a causal relationship has proven hard to establish. This is partly because much of the epidemiological evidence derives from studies of neutralising antibody generation in blood samples while less attention has been paid to the pancreatic beta cell as a site of infection. Nevertheless, recent studies have revealed that beta cells express specific enteroviral receptors and that they can sustain a productive enteroviral infection...
July 28, 2018: Current Opinion in Pharmacology
Josiah Ochieng, Gladys Nangami, Amos Sakwe, Cierra Moye, Joel Alvarez, Diva Whalen, Portia Thomas, Philip Lammers
Fetuin-A is the protein product of the AHSG gene in humans. It is mainly synthesized by the liver in adult humans and is secreted into the blood where its concentration can vary from a low of ~0.2 mg/mL to a high of ~0.8 mg/mL. Presently, it is considered to be a multifunctional protein that plays important roles in diabetes, kidney disease, and cancer, as well as in inhibition of ectopic calcification. In this review we have focused on work that has been done regarding its potential role(s) in tumor progression and sequelae of diabetes...
July 29, 2018: International Journal of Molecular Sciences
Gokhan Duruksu, Aysegul Aciksari
The microenvironment is an important factor of stem cells regulating their maintenance, survival, and differentiation. The glycation of proteins with reducing sugars through nonenzymatic reactions induces the collagen cross-linking, which causes tissue stiffening, which is enhanced during aging and diabetes. In this study, we aimed to analyze the effect of glycated collagen on the stem cell culture and differentiation. The collagen type 1 was modified by glycation with mannose, rhamnose, arabinose, and glucose...
2018: Stem Cells International
Manabu Kondo, Katsuya Tanabe, Kikuko Amo-Shiinoki, Masayuki Hatanaka, Tsukasa Morii, Harumi Takahashi, Susumu Seino, Yuichiro Yamada, Yukio Tanizawa
AIMS/HYPOTHESIS: Loss of functional beta cells results in a gradual progression of insulin insufficiency in Wolfram syndrome caused by recessive WFS1 mutations. However, beta cell dysfunction in Wolfram syndrome has yet to be fully characterised, and there are also no specific treatment recommendations. In this study, we aimed to characterise beta cell secretory defects and to examine the potential effects of a glucagon-like peptide-1 (GLP-1) receptor agonist on diabetes in Wolfram syndrome...
July 28, 2018: Diabetologia
Soren K Thomsen, Anne Raimondo, Benoit Hastoy, Shahana Sengupta, Xiao-Qing Dai, Austin Bautista, Jenny Censin, Anthony J Payne, Mahesh M Umapathysivam, Aliya F Spigelman, Amy Barrett, Christopher J Groves, Nicola L Beer, Jocelyn E Manning Fox, Mark I McCarthy, Anne Clark, Anubha Mahajan, Patrik Rorsman, Patrick E MacDonald, Anna L Gloyn
The molecular mechanisms underpinning susceptibility loci for type 2 diabetes (T2D) remain poorly understood. Coding variants in peptidylglycine α-amidating monooxygenase (PAM) are associated with both T2D risk and insulinogenic index. Here, we demonstrate that the T2D risk alleles impact negatively on overall PAM activity via defects in expression and catalytic function. PAM deficiency results in reduced insulin content and altered dynamics of insulin secretion in a human β-cell model and primary islets from cadaveric donors...
July 27, 2018: Nature Genetics
Wenli Liu, Wulin Aerbajinai, Hongzhen Li, Yueqin Liu, Oksana Gavrilova, Shalini Jain, Griffin P Rodgers
Glucose-stimulated insulin secretion (GSIS) is essential for blood glucose homeostasis and is impaired in type 2 diabetes mellitus. Understanding the regulatory components of GSIS has clinical implications for diabetes treatment. Here we found that olfactomedin 4 (OLFM4) is endogenously expressed in pancreatic islet β cells and further investigated its potential roles in glucose homeostasis and the pathogenesis of type 2 diabetes using mouse models. Olfm4-deficient mice showed significantly improved glucose tolerance and significantly increased insulin levels after glucose challenge compared with wild-type (WT) mice...
July 19, 2018: Endocrinology
Anna Dziewulska, Aneta M Dobosz, Agnieszka Dobrzyn
Type 2 diabetes (T2D) is a complex disorder that is caused by a combination of genetic, epigenetic, and environmental factors. High-throughput approaches have opened a new avenue toward a better understanding of the molecular bases of T2D. A genome-wide association studies (GWASs) identified a group of the most common susceptibility genes for T2D (i.e., TCF7L2 , PPARG , KCNJ1 , HNF1A , PTPN1 , and CDKAL1 ) and illuminated novel disease-causing pathways. Next-generation sequencing (NGS)-based techniques have shed light on rare-coding genetic variants that account for an appreciable fraction of T2D heritability ( KCNQ1 and ADRA2A ) and population risk of T2D ( SLC16A11 , TPCN2 , PAM , and CCND2 )...
July 26, 2018: Genes
Petra I Lorenzo, Nadia Cobo-Vuilleumier, Benoit R Gauthier
The high prevalence of diabetes mellitus (DM) in our society, together with the fact that current treatments are only palliative and do not prevent the development of life threatening side effects, highlights the urgent need for novel therapies targeting the root cause of the disease. Independent of the etiology of DM, the definitive therapeutic approach will imply the restitution of an adequate functional β-cell mass capable of compensating for the insulin demand of the organism. The recent demonstration of heterogeneity within the islets as well as their innate plasticity has encouraged the development of studies aiming at potentiation of the regenerative capacity of islets...
July 23, 2018: Current Opinion in Pharmacology
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