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https://www.readbyqxmd.com/read/29784660/interleukin-6-reduces-%C3%AE-cell-oxidative-stress-by-linking-autophagy-with-the-antioxidant-response
#1
Michelle R Marasco, Abass M Conteh, Christopher A Reissaus, John E Cupit V, Evan M Appleman, Raghavendra G Mirmira, Amelia K Linnemann
Production of reactive oxygen species (ROS) is a key instigator of β-cell dysfunction in diabetes. The pleiotropic cytokine IL-6 has previously been linked to β-cell autophagy but has not been studied in the context of β-cell antioxidant response. We used a combination of animal models of diabetes and analysis of cultured human islets and rodent β-cells to study how IL-6 influences antioxidant response. We show that IL-6 couples autophagy to antioxidant response to reduce β-cell and human islet ROS. β cell-specific loss of IL-6 signaling in vivo renders mice more susceptible to oxidative damage and cell death by the selective β-cell toxins streptozotocin and alloxan...
May 21, 2018: Diabetes
https://www.readbyqxmd.com/read/29779190/therapeutic-strategies-for-modulating-the-extracellular-matrix-to-improve-pancreatic-islet-function-and-survival-after-transplantation
#2
REVIEW
Alexandra M Smink, Paul de Vos
PURPOSES OF REVIEW: Extracellular matrix (ECM) components modulate the interaction between pancreatic islet cells. During the islet isolation prior to transplantation as treatment for type 1 diabetes, the ECM is disrupted impacting functional graft survival. Recently, strategies for restoring ECM have shown to improve transplantation outcomes. This review discusses the current therapeutic strategies to modulate ECM components to improve islet engraftment. RECENT FINDINGS: Approaches applied are seeding islets in ECM of decellularized organs, supplementation of specific ECM components in polymeric scaffolds or immunoisolating capsules, and stimulating islet ECM production with specific growth factors or ECM-producing cells...
May 19, 2018: Current Diabetes Reports
https://www.readbyqxmd.com/read/29765322/therapeutic-potential-of-ginsenosides-as-an-adjuvant-treatment-for-diabetes
#3
REVIEW
Litao Bai, Jialiang Gao, Fan Wei, Jing Zhao, Danwei Wang, Junping Wei
Ginseng, one of the oldest traditional Chinese medicinal herbs, has been used widely in China and Asia for thousands of years. Ginsenosides extracted from ginseng, which is derived from the roots and rhizomes of Panax ginseng C. A. Meyer, have been used in China as an adjuvant in the treatment of diabetes mellitus. Owing to the technical complexity of ginsenoside production, the total ginsenosides are generally extracted. Accumulating evidence has shown that ginsenosides exert antidiabetic effects. In vivo and in vitro tests revealed the potential of ginsenoside Rg1, Rg3, Rg5, Rb1, Rb2, Rb3, compound K, Rk1, Re, ginseng total saponins, malonyl ginsenosides, Rd, Rh2, F2, protopanaxadiol (PPD) and protopanaxatriol (PPT)-type saponins to treat diabetes and its complications, including type 1 diabetes mellitus, type 2 diabetes mellitus, diabetic nephropathy, diabetic cognitive dysfunction, type 2 diabetes mellitus with fatty liver disease, diabetic cerebral infarction, diabetic cardiomyopathy, and diabetic erectile dysfunction...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29753073/glycine-transporter-1-and-glycine-receptor-mediate-the-antioxidant-effect-of-glycine-in-diabetic-rat-islets-and-ins-1-cells
#4
Lei Chen, Junqing Zhang, Changhong Li, Ziwei Wang, Jingjing Li, Dan Zhao, Suxia Wang, Hong Zhang, Youyuan Huang, Xiaohui Guo
Oxidative stress is the main inducer of β-cell damage, which underlies the pathogenesis of diabetes. Evidence suggests that glycine, a recognized antioxidant, may improve β-cell function; however, its mechanism in protecting diabetic β-cells against oxidative stress has not been directly investigated. Using a streptozotocin-induced diabetic rat model and INS-1 pancreatic β-cells, we evaluated whether glycine can attenuate diabetic β-cell damage induced by oxidative stress. In diabetic rats, glycine stimulated insulin secretion; enhanced plasma glutathione (GSH), catalase and superoxide dismutase levels; reduced plasma 8-hydroxy-2 deoxyguanosine and islet p22phox levels; and improved islet β-cell mitochondrial degeneration and insulin granule degranulation...
May 9, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29749717/using-mesenchymal-stromal-cells-in-islet-transplantation
#5
EDITORIAL
Ahmed A Arzouni, Andreia Vargas-Seymour, Nance Nardi, Aileen J F King, Peter M Jones
Islet transplantation has the potential to cure Type 1 diabetes but current clinical transplantation protocols are inefficient because of the extensive loss of functional islets during the immediate post-transplantation period. Studies in rodent models have demonstrated that co-transplanting mesencyhmal stromal cells (MSCs) with islets improves graft functional survival and transplantation outcomes, and some of the beneficial effects of MSCs are attributable to bioactive molecules secreted by MSCs. Clinical islet transplantation is almost exclusively via the hepatic portal vein, which does not facilitate co-engraftment of islets and MSCs so attention is currently focused on using cell-free cocktails of MSC-derived products to treat islets prior to transplantation...
May 11, 2018: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/29740396/redox-dependent-inflammation-in-islet-transplantation-rejection
#6
REVIEW
Jessie M Barra, Hubert M Tse
Type 1 diabetes is an autoimmune disease that results in the progressive destruction of insulin-producing pancreatic β-cells inside the islets of Langerhans. The loss of this vital population leaves patients with a lifelong dependency on exogenous insulin and puts them at risk for life-threatening complications. One method being investigated to help restore insulin independence in these patients is islet cell transplantation. However, challenges associated with transplant rejection and islet viability have prevented long-term β-cell function...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29725251/glucagon-like-peptide-1-receptor-agonist-and-glucagon-increase-glucose-stimulated-insulin-secretion-in-beta-cells-via-distinct-adenylyl-cyclases
#7
Young-Sun Lee, Hee-Sook Jun
Diabetes mellitus is a chronic disease in which the pancreas no longer produces enough insulin. Pancreatic alpha cell mass increases in response to insufficient insulin secretion. However, the reason for this increase is not clear. It is possible that the increased alpha-cells may stimulate compensatory insulin release in response to the insufficient insulin such as insulin resistance. In this study, we investigated whether glucagon and glucagon-like peptide-1 (GLP-1), hormones produced by alpha cells, contribute to insulin secretion in INS-1 cells, a beta cell line...
2018: International Journal of Medical Sciences
https://www.readbyqxmd.com/read/29717931/-re-generating-human-beta-cells-status-pitfalls-and-perspectives
#8
Luc Baeyens, Marie Lemper, Willem Staels, Sofie De Groef, Nico De Leu, Yves Heremans, Michael S German, Harry Heimberg
Diabetes mellitus results from disturbed glucose homeostasis due to an absolute (type 1) or relative (type 2) deficiency of insulin, a peptide hormone almost exclusively produced by the beta cells of the endocrine pancreas in a tightly regulated manner. Current therapy only delays disease progression through insulin injection and/or oral medications that increase insulin secretion or sensitivity, decrease hepatic glucose production, or promote glucosuria. These drugs have turned diabetes into a chronic disease as they do not solve the underlying beta cell defects or entirely prevent the long-term complications of hyperglycemia...
July 1, 2018: Physiological Reviews
https://www.readbyqxmd.com/read/29707204/loss-of-zbtb32-in-nod-mice-does-not-significantly-alter-t-cell-responses
#9
William D Coley, Yongge Zhao, Charles J Benck, Yi Liu, Chie Hotta-Iwamura, M Jubayer Rahman, Kristin V Tarbell
Background : We previously identified the transcriptional regulator Zbtb32 as a factor that can promote T cell tolerance in the Non-Obese Diabetic (NOD) mouse, a model of Type 1 diabetes. Antigen targeted to DCIR2 + dendritic cells (DCs) in vivo inhibited both diabetes and effector T cell expansion in NOD mice. Furthermore, Zbtb32 was preferentially induced in autoreactive CD4 T cells stimulated by these tolerogenic DCIR2 + DCs, and overexpression of Zbtb32 in islet-specific T cells inhibited the diabetes development by limiting T cell proliferation and cytokine production...
2018: F1000Research
https://www.readbyqxmd.com/read/29705815/pancreatic-%C3%AE-cells-overexpressing-hiapp-impaired-mitophagy-and-unbalanced-mitochondrial-dynamics
#10
Miriam García Hernández, Ana García Aguilar, Jesús Burillo, Raquel Gómez Oca, Maria Antonietta Manca, Ana Novials, Gema Alcarraz-Vizan, Carlos Guillén, Manuel Benito
Human islet amyloid polypeptide (hIAPP), or amylin, has the tendency to aggregate into insoluble amyloid fibrils, a typical feature of islets from type 2 diabetes individuals. Thus, we investigated comparatively the impact of hIAPP on key pathways involved in pancreatic beta survival. INS1E-hIAPP cells present a hyperactivation of MTORC1 and an inhibition of autophagy signaling, those cells showing an increase in cell size. Resveratrol, a MTORC1 inhibitor, can reverse TSC2 degradation that occurs in INS1E-hIAPP cells and diminished MTORC1 hyperactivation with concomitant autophagy stimulation...
April 29, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29694904/%C3%AE-cell-glp-1r-signaling-alters-%C3%AE-cell-proglucagon-processing-after-vertical-sleeve-gastrectomy-in-mice
#11
Darline Garibay, Jon Lou, Seon A Lee, Karolina E Zaborska, Margot H Weissman, Erica Sloma, Leanne Donahue, Andrew D Miller, Andrew C White, M Dodson Michael, Kyle W Sloop, Bethany P Cummings
Bariatric surgery, such as vertical sleeve gastrectomy (VSG), causes high rates of type 2 diabetes remission and remarkable increases in postprandial glucagon-like peptide-1 (GLP-1) secretion. GLP-1 plays a critical role in islet function by potentiating glucose-stimulated insulin secretion; however, the mechanisms remain incompletely defined. Therefore, we applied a murine VSG model to an inducible β cell-specific GLP-1 receptor (GLP-1R) knockout mouse model to investigate the role of the β cell GLP-1R in islet function...
April 24, 2018: Cell Reports
https://www.readbyqxmd.com/read/29691580/-adenovirus-mediated-overexpression-of-thioredoxin-interaction-protein-inhibits-ins-1-islet-%C3%AE-cell-proliferation
#12
Zhu-Jie Cao, Yan-Jin Feng, Dan Li, Jin Wang, Hai-Yan Huo, Xu-Mei Zhang, Xiang-Ying Jiao
Diabetes can cause a significant increase in the expression of thioredoxin (Trx)-interacting protein (TXNIP), which binds to Trx and inhibits its activity. The present study was aimed to investigate the effect of TXNIP on proliferation of rat INS-1 islet β cells and the underlying mechanism. TXNIP overexpressing adenovirus vectors (Ad-TXNIP-GFP and Ad-TXNIPc247s-GFP) were constructed and used to infect INS-1 cells. Ad-TXNIPc247s-GFP vector carries a mutant C247S TXNIP gene, and its expression product (TXNIPc247s) cannot attach and inhibit Trx activity...
April 25, 2018: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/29670917/pancreatic-beta-cell-death-novel-potential-mechanisms-in-diabetes-therapy
#13
REVIEW
Joselyn Rojas, Valmore Bermudez, Jim Palmar, María Sofía Martínez, Luis Carlos Olivar, Manuel Nava, Daniel Tomey, Milagros Rojas, Juan Salazar, Carlos Garicano, Manuel Velasco
Purpose of Review: Describing the diverse molecular mechanisms (particularly immunological) involved in the death of the pancreatic beta cell in type 1 and type 2 diabetes mellitus. Recent Findings: Beta cell death is the final event in a series of mechanisms that, up to date, have not been entirely clarified; it represents the pathophysiological mechanism in the natural history of diabetes mellitus. These mechanisms are not limited to an apoptotic process only, which is characteristic of the immune-mediated insulitis in type 1 diabetes mellitus...
2018: Journal of Diabetes Research
https://www.readbyqxmd.com/read/29665055/s6k1-controls-epigenetic-plasticity-for-the-expression-of-pancreatic-%C3%AE-%C3%AE-cell-marker-genes
#14
Sang Ah Yi, Jieun Lee, Jong Woo Park, Jihoon Han, Min Gyu Lee, Ki Hong Nam, Jee Hun Park, Hwamok Oh, Sung Jin Ahn, Saetbyul Kim, So Hee Kwon, Dong-Gyu Jo, Jeung-Whan Han
The failure of insulin production by pancreatic β cells is a common hallmark of type 1 diabetes mellitus (T1DM). Because administration of exogenous insulin is associated with diabetes-derived complications, endogenous α to β cell transition can be an attractive alternative. Although decreased β cell size and hypoinsulinaemia have been observed in S6K1-deficient mice, the molecular mechanism underlying the involvement of S6K1 in the transcriptional regulation of insulin remains elusive. Here, we show that the hypoinsulinaemic phenotype of S6K1-deficient mice stems from the dysregulated transcription of a set of genes required for insulin and glucagon production...
April 17, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29664925/actin-and-myosin-ii-modulate-differentiation-of-pluripotent-stem-cells
#15
Liana C Boraas, Emma T Pineda, Tabassum Ahsan
Use of stem cell-based therapies in tissue engineering and regenerative medicine is hindered by efficient means of directed differentiation. For pluripotent stem cells, an initial critical differentiation event is specification to one of three germ lineages: endoderm, mesoderm, and ectoderm. Differentiation is known to be regulated by numerous extracellular and intracellular factors, but the role of the cytoskeleton during specification, or early differentiation, is still unknown. In these studies, we used agonists and antagonists to modulate actin polymerization and the actin-myosin molecular motor during spontaneous differentiation of embryonic stem cells in embryoid bodies...
2018: PloS One
https://www.readbyqxmd.com/read/29664151/the-receptor-for-advanced-glycation-endproducts-is-a-mediator-of-toxicity-by-iapp-and-other-proteotoxic-aggregates-establishing-and-exploiting-common-ground-for-novel-amyloidosis-therapies
#16
REVIEW
Andisheh Abedini, Julia Derk, Ann Marie Schmidt
Proteotoxicity plays a key role in many devastating human disorders, including Alzheimer's, Huntington's and Parkinson's diseases; type 2 diabetes; systemic amyloidosis; and cardiac dysfunction, to name a few. The cellular mechanisms of proteotoxicity in these disorders have been the focus of considerable research, but their role in prevalent and morbid disorders, such as diabetes, is less appreciated. There is a large body of literature on the impact of glucotoxicity and lipotoxicity on insulin-producing pancreatic β-cells, and there is increasing recognition that proteotoxicty plays a key role...
April 17, 2018: Protein Science: a Publication of the Protein Society
https://www.readbyqxmd.com/read/29658605/aerobic-exercise-regulates-blood-lipid-and-insulin-resistance-via-the-toll%C3%A2-like-receptor-4%C3%A2-mediated-extracellular-signal%C3%A2-regulated-kinases-amp%C3%A2-activated-protein-kinases-signaling-pathway
#17
Mei Wang, Sen Li, Fubaihui Wang, Jinhui Zou, Yanfeng Zhang
Diabetes mellitus is a complicated metabolic disease with symptoms of hyperglycemia, insulin resistance, chronic damage and dysfunction of tissues, and metabolic syndrome for insufficient insulin production. Evidence has indicated that exercise treatments are essential in the progression of type‑ІІ diabetes mellitus, and affect insulin resistance and activity of islet β‑cells. In the present study, the efficacy and signaling mechanism of aerobic exercise on blood lipids and insulin resistance were investigated in the progression of type‑ІІ diabetes mellitus...
April 11, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29649104/coordination-of-gpr40-and-ketogenesis-signaling-by-medium-chain-fatty-acids-regulates-beta-cell-function
#18
Julien Benjamin Pujol, Nicolas Christinat, Yann Ratinaud, Claudia Savoia, Siobhan E Mitchell, El Hadji M Dioum
Diabetes prevalence increases with age, and β-cell dysfunction contributes to the incidence of the disease. Dietary lipids have been recognized as contributory factors in the development and progression of the disease. Unlike long chain triglycerides, medium chain triglycerides (MCT) increase fat burning in animal and human subjects as well as serum C-peptide in type 2 diabetes patients. We evaluated the beneficial effects of MCT on β-cells in vivo and in vitro. MCT improved glycemia in aged rats via β-cell function assessed by measuring insulin secretion and content...
April 12, 2018: Nutrients
https://www.readbyqxmd.com/read/29643912/association-of-rage-gene-polymorphism-with-type-2-diabetes-mellitus-in-local-population
#19
Saba Zulfiqar, Fatma Hussain, Amer Jamil, Nisar Ahmed
Objectives: Type-2 diabetes mellitus (T2DM) is an endocrine disease having a significant genetic component. Polymorphisms of many genes may affect hereditary vulnerability of the disease that is characterized by insulin resistance and islet disorder. As the genetic basis of T2DM can vary between ethnic groups, it is important to investigate the genetic link of T2DM in Pakistani populace. This study was aimed to assess the association of receptor for advanced glycation end product (RAGE) gene polymorphism (-429T>C) with Type-2 diabetes mellitus within local populace...
January 2018: Pakistan Journal of Medical Sciences Quarterly
https://www.readbyqxmd.com/read/29627328/toxoplasma-gondii-as-a-possible-causative-pathogen-of-type-1-diabetes-mellitus-evidence-from-case-control-and-experimental-studies
#20
Engy Victor Nassief Beshay, Samar A El-Refai, Mohamed A Helwa, Amany Fawzy Atia, Marwa Mohammed Dawoud
Toxoplasma gondii is the causative parasite of an important worldwide disease. This obligate intracellular parasite can infect and replicate inside any nucleated cells including those of pancreas. Insulin is a hormone secreted by the pancreas and is responsible for controlling blood glucose concentration. Deficiency of insulin production accounts for the occurrence of type-1 diabetes mellitus (T1D). Thus, theoretically, toxoplasmosis could play a possible role in the development of T1D. However, the studies on this theory are still insufficient; therefore, this work was designed...
May 2018: Experimental Parasitology
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