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er stress and diabetes

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https://www.readbyqxmd.com/read/29160038/endoplasmic-reticulum-in-health-and-disease-the-12th-international-calreticulin-workshop-delphi-greece
#1
REVIEW
Aristidis S Charonis, Marek Michalak, Jody Groenendyk, Luis B Agellon
Starting from 1994, every 2 years, an international workshop is organized focused on calreticulin and other endoplasmic reticulum chaperones. In 2017, the workshop took place at Delphi Greece. Participants from North and South America, Europe, Asia and Australia presented their recent data and discussed them extensively with their colleagues. Presentations dealt with structural aspects of calreticulin and calnexin, the role of Ca(2+) in cellular signalling and in autophagy, the endoplasmic reticulum stress and the unfolded protein response, the role of calreticulin in immune responses...
November 21, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29147529/ratiometric-photoacoustic-imaging-of-endoplasmic-reticulum-polarity-in-injured-liver-tissues-of-diabetic-mice
#2
Haibin Xiao, Chuanchen Wu, Ping Li, Wen Gao, Wen Zhang, Wei Zhang, Lili Tong, Bo Tang
As one of the complications of diabetes, liver injury results in significant hazards. Therefore, accurately diagnosing diabetes-induced liver injury beforehand is crucial for the warning and treatment of hepatic diseases. Diabetes-induced liver injury can cause changes in the microstructure and morphology of liver tissue, leading to changes in the hydrophilic and hydrophobic domains in the endoplasmic reticulum (ER), which is closely associated with changes in cellular ER polarity. So, differences in the ER polarity can indicate the degree of diabetes-induced liver injury...
October 1, 2017: Chemical Science
https://www.readbyqxmd.com/read/29133483/ctage5-deletion-in-pancreatic-%C3%AE-cells-impairs-proinsulin-trafficking-and-insulin-biogenesis-in-mice
#3
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/29133342/exercise-training-protects-human-and-rodent-%C3%AE-cells-against-endoplasmic-reticulum-stress-and-apoptosis
#4
Flavia M M Paula, Nayara C Leite, Patricia C Borck, Ricardo Freitas-Dias, Miriam Cnop, Mara P T Chacon-Mikahil, Claudia R Cavaglieri, Piero Marchetti, Antonio C Boschero, Claudio C Zoppi, Decio L Eizirik
Prolonged exercise has positive metabolic effects in obese or diabetic individuals. These effects are usually ascribed to improvements in insulin sensitivity. We evaluated whether exercise also generates circulating signals that protect human and rodent β cells against endoplasmic reticulum (ER) stress and apoptosis. For this purpose, we obtained serum from humans or mice before and after an 8 wk training period. Exposure of human islets or mouse or rat β cells to human or rodent sera, respectively, obtained from trained individuals reduced cytokine (IL-1β+IFN-γ)- or chemical ER stressor-induced β-cell ER stress and apoptosis, at least in part via activation of the transcription factor STAT3...
November 13, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29129775/connecting-alzheimer-s-disease-to-diabetes-underlying-mechanisms-and-potential-therapeutic-targets
#5
REVIEW
Marcelo N N Vieira, Ricardo A S Lima-Filho, Fernanda G De Felice
Alzheimer's disease (AD) is a risk factor for type 2 diabetes and vice versa, and a growing body of evidence indicates that these diseases are connected both at epidemiological, clinical and molecular levels. Recent studies have begun to reveal common pathogenic mechanisms shared by AD and type 2 diabetes. Impaired neuronal insulin signaling and endoplasmic reticulum (ER) stress are present in animal models of AD, similar to observations in peripheral tissue in T2D. These findings shed light into novel diabetes-related mechanisms leading to brain dysfunction in AD...
November 9, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/29115440/aspirin-ameliorates-cerebral-infarction-through-regulation-of-tlr4-nf%C3%A2-%C3%AE%C2%BAb%C3%A2-mediated-endoplasmic-reticulum-stress-in-mouse-model
#6
Xin Wang, Bin Shen, Dezhou Sun, Xiangyu Cui
Cerebral infarction is a cerebrovascular disease caused by local brain ischemic necrosis or softening, which is associated with diabetes, obesity, hypertension and rheumatic heart arrhythmia. Previous studies have indicated that aspirin is a potential oral anticoagulant in the treatment of cerebral ischemic stroke. However, the potential mechanism mediated by aspirin in cerebral infarction therapy is not well understood. The present study analyzed the therapeutic effects of aspirin on cerebral infarction and investigated the underlying molecular mechanism of aspirin‑ameliorated benefits for thrombolysis...
October 25, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115422/melatonin-ameliorates-myocardial-apoptosis-by-suppressing-endoplasmic-reticulum-stress-in-rats-with-long%C3%A2-term-diabetic-cardiomyopathy
#7
Fang-Yuan Xiong, Song-Tao Tang, Huan Su, Hai-Qin Tang, Pin Jiang, Qing Zhou, Yuan Wang, Hua-Qing Zhu
The effects of melatonin (MLT), which exerts cardioprotective effects against myocardial apoptosis, in long‑term diabetic cardiomyopathy are not currently well defined. The present study aimed to investigate how MLT protects the heart through modulating myocardial apoptosis in rats with type 2 diabetes mellitus (DM). In total, 36 rats were randomly divided into three groups, including control (n=12), DM (n=12) and DM + MLT (n=12) groups. The results demonstrated that, in DM rats, a significant increase was observed in the serum fasting blood glucose and lipid levels, in addition to insulin resistance and cardiac dysfunction, which were attenuated in DM rats treated with MLT...
October 20, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29113994/hepatocyte-specific-deletion-of-bap31-promotes-srebp1c-activation-promotes-hepatic-lipid-accumulation-and-worsens-insulin-resistance-in-mice
#8
Jia-Lin Xu, Li-Ya Li, Yan-Qing Wang, Ya-Qi Li, Mu Shan, Shi-Zhuo Sun, Yang Yu, Bing Wang
Conditional knockout mice with targeted disruption of BAP31 in adult mouse liver were generated and challenged with a high-fat diet (HFD) for 36 or 96 days, markers of obesity, diabetes, and hepatic steatosis were determined. Mutant mice were indistinguishable from wild-type littermates, but exhibited increased HFD-induced obesity. BAP31-deletion in hepatocytes increased the expression of SREBP1C and the target genes, including ACC1 and SCD1, increased hepatic lipid accumulation and HFD-induced liver steatosis...
November 7, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/29111283/pancreatic-islet-autonomous-effect-of-arsenic-on-insulin-secretion-through-endoplasmic-reticulum-stress-autophagy-pathway
#9
Wei Wu, Xiaofeng Yao, Liping Jiang, Qiaoting Zhang, Jie Bai, Tianming Qiu, Lei Yang, Ni Gao, Guang Yang, Xiaofang Liu, Min Chen, Xiance Sun
Inorganic arsenic is a worldwide environmental pollutant. Arsenic's relationship with the incidence of diabetes arouses concerns on its etiological mechanism. In this study, the glucose-stimulated insulin secretion (GSIS) from isolated pancreatic islets of As2O3-treated mice was significantly lower than that of control mice. It indicated that the effect of As2O3-inhibited GSIS was pancreatic islet-autonomous. The level of phospho-PERK (p-PERK), a biomarker of endoplasmic reticulum (ER) stress, in pancreas of As2O3-treated mice was increased significantly...
October 27, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/29111234/exacerbation-and-prolongation-of-psoriasiform-inflammation-in-diabetic-obese-mice-a-synergistic-role-of-cxcl5-and-er-stress
#10
Noriko Shimoura, Hiroshi Nagai, Susumu Fujiwara, Haruki Jimbo, Chikako Nishigori
Accumulating evidence suggests that psoriasis is frequently accompanied by metabolic disorders such as obesity and diabetes. However, the mechanisms underlying the association between increased psoriasis severity and concomitant metabolic syndrome have not been fully clarified. Herein, we show that imiquimod-induced psoriasiform inflammation was exacerbated and prolonged in diabetic obese mice compared to that in control mice, accompanied by remarkably increased lesional expressions of Cxcl5 and Il-1b. Notably, a large number of CXCL5(+) Ly6G(+) cells infiltrated the dermis and subcutaneous fat tissue of the diabetic obese mice...
October 27, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29107536/the-unfolded-protein-response-and-cell-fate-control
#11
REVIEW
Claudio Hetz, Feroz R Papa
The secretory capacity of a cell is constantly challenged by physiological demands and pathological perturbations. To adjust and match the protein-folding capacity of the endoplasmic reticulum (ER) to changing secretory needs, cells employ a dynamic intracellular signaling pathway known as the unfolded protein response (UPR). Homeostatic activation of the UPR enforces adaptive programs that modulate and augment key aspects of the entire secretory pathway, whereas maladaptive UPR outputs trigger apoptosis. Here, we discuss recent advances into how the UPR integrates information about the intensity and duration of ER stress stimuli in order to control cell fate...
October 25, 2017: Molecular Cell
https://www.readbyqxmd.com/read/29104496/diabetes-induces-abnormal-ovarian-function-via-triggering-apoptosis-of-granulosa-cells-and-suppressing-ovarian-angiogenesis
#12
Yanqing Wu, Yiyang Li, Xinghui Liao, Zhengchao Wang, Rui Li, Shuang Zou, Ting Jiang, Bingbing Zheng, Ping Duan, Jian Xiao
Diabetes triggers abnormal ovarian follicular development and consequently leads to infertility. Here, we established a type 2 diabetes mouse model by feeding with high fat diet (HFD) for 15/20 weeks and assessed the effect of diabetes on follicular development and ovarian angiogenesis. After fed with HFD for 15 weeks, mice had the characteristics of type 2 diabetes, which was much more serious after 20 weeks on HFD. After 20 weeks on HFD, the mice had shown abnormal ovarian morphology with hyaline appearance, much less blood vessel, follicular development arrest and less of granulosa cells (GCs) in mature follicles, but not in ovaries from 15 weeks on HFD...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/29081894/the-contribution-of-singlet-oxygen-to-insulin-resistance
#13
REVIEW
Arnold N Onyango
Insulin resistance contributes to the development of diabetes and cardiovascular dysfunctions. Recent studies showed that elevated singlet oxygen-mediated lipid peroxidation precedes and predicts diet-induced insulin resistance (IR), and neutrophils were suggested to be responsible for such singlet oxygen production. This review highlights literature suggesting that insulin-responsive cells such as endothelial cells, hepatocytes, adipocytes, and myocytes also produce singlet oxygen, which contributes to insulin resistance, for example, by generating bioactive aldehydes, inducing endoplasmic reticulum (ER) stress, and modifying mitochondrial DNA...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29081777/hyperglycemia-aggravates-hepatic-ischemia-and-reperfusion-injury-by-inhibiting-liver-resident-macrophage-m2-polarization-via-c-ebp-homologous-protein-mediated-endoplasmic-reticulum-stress
#14
Zhuqing Rao, Jie Sun, Xiongxiong Pan, Ziyang Chen, Heliang Sun, Panpan Zhang, Mei Gao, Zhengnian Ding, Cunming Liu
Aggravated liver ischemia and reperfusion (IR) injury has been observed in hyperglycemic hosts, but its underlying mechanism remains undefined. Liver-resident macrophages (Kupffer cells, KCs) and endoplasmic reticulum (ER) stress play crucial roles in the pathogenesis of liver IR injury. In this study, we evaluated the role of ER stress in regulating KC activation and liver IR injury in a streptozotocin-induced hyperglycemic/diabetic mouse model. Compared to the control group (CON group), hyperglycemic mice exhibited a significant increase in liver injury and intrahepatic inflammation following IR...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29079731/involvement-of-er-stress-pi3k-akt-activation-and-lung-fibroblast-proliferation-in-bleomycin-induced-pulmonary-fibrosis
#15
Han-Shui Hsu, Chen-Chi Liu, Jiun-Han Lin, Tien-Wei Hsu, Jyuan-Wei Hsu, Kelly Su, Shih-Chieh Hung
Pulmonary fibrosis is characterized by fibroblast proliferation and extracellular matrix remodelling, leading to respiratory insufficiency. The mechanisms underlying this progressive and devastating disease remain unclear. Conditions that can impair the function of the endoplasmic reticulum (ER) cause accumulation of unfolded or misfolded proteins, resulting in ER stress and activation of the unfolded protein response (UPR). ER stress has been implicated in many conditions including cancer, diabetes, obesity, and inflammation...
October 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29079192/exposure-to-cigarette-smoke-disturbs-adipokines-secretion-causing-intercellular-damage-and-insulin-resistance-in-high-fructose-diet-induced-metabolic-disorder-mice
#16
Sanghwa Kim, Ah Young Lee, Hyeon-Jeong Kim, Seong-Ho Hong, Ryeo-Eun Go, Kyung-Chul Choi, Kyung-Sun Kang, Myung-Haing Cho
A large amount of fructose intake along with smoking is associated with increased incidence of diseases linked to metabolic syndrome. More research is necessary to understand the complex mechanism that ultimately results in metabolic syndrome and the effect, if any, of high fructose dietary intake and smoking on individual health. In this study, we investigated changes in ER-Golgi network and disturbance to secretion of adipokines induced by cigarette smoking (CS) and excess fructose intake and their contribution to the disruption of metabolic homeostasis...
October 25, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29070677/overexpression-of-sphingosine-1-phosphate-lyase-protects-insulin-secreting-cells-against-cytokine-toxicity
#17
Claudine Hahn, Karolina Tyka, Julie D Saba, Sigurd Lenzen, Ewa Gurgul-Convey
Increasing evidence suggests a crucial role of inflammation in cytokine-mediated β-cell dysfunction and death in type-1 diabetes (T1DM), though the mechanisms are incompletely understood. Sphingosine-1 phosphate (S1P) is a multifunctional bioactive sphingolipid involved in the development of many autoimmune and inflammatory diseases. Here, we investigated the role of intracellular S1P in insulin-secreting INS1E cells by genetically manipulating the S1P-metabolizing enzyme S1P lyase (SPL). The expression of SPL was downregulated by cytokines in INS1E cells and rat islets...
October 25, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29061071/does-metformin-modulate-endoplasmic-reticulum-stress-and-autophagy-in-type-2-diabetic-pbmcs
#18
Noelia Diaz-Morales, Francesca Iannantuoni, Irene Escribano-Lopez, Celia Bañuls, Susana Rovira-Llopis, Eva Sola, Milagros Rocha, Antonio Hernandez-Mijares, Victor M Victor
Since type 2 diabetes (T2D) is closely associated with enhanced oxidative stress and metformin has been shown to exert a protective role against said stress, we posed the question of whether metformin treatment might also modulate endoplasmic reticulum (ER) stress and autophagy in leukocytes of T2D patients. We studied 53 T2D patients (37 of whom had been treated with metformin 1700mg for at least 1 year) and 30 healthy volunteers. Whereas leukocytes from both groups of T2D patients exhibited increased protein levels of GRP78 with respect to controls, ATF6 was enhanced specifically in non-metformin-treated T2D, while <i>s-xbp1</i> and p-eIF2α increased only in the metformin-treated group...
October 23, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29040818/metformin-attenuates-er-stress-induced-mitochondrial-dysfunction
#19
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress, a disturbance of the ER function, contributes to cardiac injury. ER and mitochondria are closely connected organelles within cells. ER stress contributes to mitochondrial dysfunction, which is a key factor to increase cardiac injury. Metformin, a traditional anti-diabetic drug, decreases cardiac injury during ischemia-reperfusion. Metformin also inhibits ER stress in cultured cells. We hypothesized that metformin can attenuate the ER stress-induced mitochondrial dysfunction and subsequent cardiac injury...
September 28, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29033899/environmental-factors-contribute-to-%C3%AE-cell-endoplasmic-reticulum-stress-and-neo-antigen-formation-in-type-1-diabetes
#20
Meghan L Marré, Jon D Piganelli
Type 1 diabetes (T1D) is an autoimmune disease in which immune-mediated targeting and destruction of insulin-producing pancreatic islet β cells leads to chronic hyperglycemia. There are many β cell proteins that are targeted by autoreactive T cells in their native state. However, recent studies have demonstrated that many β cell proteins are recognized as neo-antigens following posttranslational modification (PTM). Although modified neo-antigens are well-established targets of pathology in other autoimmune diseases, the effects of neo-antigens in T1D progression and the mechanisms by which they are generated are not well understood...
2017: Frontiers in Endocrinology
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