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er stress and diabetes

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https://www.readbyqxmd.com/read/27914514/protective-effects-of-fish-oil-and-pioglitazone-on-pancreatic-tissue-in-obese-kk-mice-with-type-2-diabetes
#1
Yuzuru Iizuka, Hyounju Kim, Takuya Izawa, Koji Sakurai, Satoshi Hirako, Masahiro Wada, Akiyo Matsumoto
n-3 Polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have protective effects against the pancreatic β-cell dysfunction through several mechanisms. Thiazolidines are insulin sensitizers and are used in treating patients with type 2 diabetes. Our previous study demonstrated that a combination of fish oil, which is rich with EPA and DHA, and pioglitazone exerts beneficial effects on obesity and diabetes through their actions on the liver and adipose tissue. However, it remains largely unknown whether such combination therapy affects the pancreas...
December 2016: Prostaglandins, Leukotrienes, and Essential Fatty Acids
https://www.readbyqxmd.com/read/27909574/characterization-of-5-2-18-f-fluoroethoxy-l-tryptophan-for-pet-imaging-of-the-pancreas
#2
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/27879249/glucosamine-induces-er-stress-by-disrupting-lipid-linked-oligosaccharide-biosynthesis-and-n-linked-protein-glycosylation
#3
Daniel R Beriault, Vi T Dang, Lexy H Zhong, Christina I Petlura, Cameron S McAlpine, Yuanyuan Shi, Geoff H Werstuck
Glucosamine is an essential substrate for N-linked protein glycosylation. However, elevated levels of glucosamine can induce endoplasmic reticulum (ER) stress. Glucosamine-induced ER stress has been implicated in the development of diabetic complications including atherosclerosis and hepatic steatosis. In this study, we investigate the potential relationship between the effects of glucosamine on lipid linked oligosaccharide (LLO) biosynthesis, N-linked glycosylation, and ER homeostasis. Mouse embryonic fibroblasts (MEFs) were cultured in the presence of 0-5 mM glucosamine for up to 18 hours and LLO biosynthesis was monitored by fluorescence-assisted carbohydrate electrophoresis...
November 22, 2016: American Journal of Physiology. Endocrinology and Metabolism
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
#4
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/27871808/new-mechanism-of-lipotoxicity-in-diabetic-cardiomyopathy-deficiency-of-endogenous-h2s-production-and-er-stress
#5
Runmin Guo, Zijun Wu, Jiamei Jiang, Chang Liu, Bin Wu, Xingyue Li, Teng Li, Hailiang Mo, Songjian He, Shanghai Li, Hai Yan, Ruina Huang, Qiong You, Keng Wu
OBJECTIVE: To investigate the roles and mechanisms of endogenous hydrogen sulfide (H2S) and endoplasmic reticulum (ER) stress in the development of diabetic cardiomyopathy (DCM). METHODS: Blood of DCM patients included in the study were collected. The model of DCM rats was established using streptozotocin (STZ) injection. Cardiac lipotoxicity in vitro models were established using 500μM palmitic acid (PA) treatment for 24h in AC16 cardiomyocytes. Endogenous H2S production in plasma, culture supernatant and heart was measured by sulphur ion-selective electrode assay...
November 18, 2016: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/27859785/increased-monocyte-derived-reactive-oxygen-species-in-type-2-diabetes-role-of-endoplasmic-reticulum-stress
#6
Robert M Restaino, Shekhar H Deo, Alan R Parrish, Paul J Fadel, Jaume Padilla
Recent evidence suggests that exposure of human monocytes to glucolipotoxic media to mimic the composition of plasma of patients with type 2 diabetes (T2D) results in the induction of endoplasmic reticulum stress markers and formation of reactive oxygen species (ROS). The extent to which these findings translate to patients with T2D remains unclear. Thus, we first measured ROS (dihydroethidium fluorescence) in peripheral blood mononuclear cells (PBMCs) from whole blood of T2D patients (n = 8) and compared to age matched healthy controls (n = 8)...
November 18, 2016: Experimental Physiology
https://www.readbyqxmd.com/read/27856609/ppar%C3%AE-is-required-for-exercise-to-attenuate-endoplasmic-reticulum-stress-and-endothelial-dysfunction-in-diabetic-mice
#7
Wai San Cheang, Wing Tak Wong, Lei Zhao, Jian Xu, Li Wang, Chi Wai Lau, Zhen Yu Chen, Ronald Ching Wan Ma, Aimin Xu, Nanping Wang, Xiao Yu Tian, Yu Huang
Physical activity has profound benefits on health especially cardiometablic wellness. Experiments on rodents with trained exercise showed that exercise improves vascular function and reduces vascular inflammation by modulating the balance between nitric oxide (NO) and oxidative stress. However, it is unclear what is the upstream regulator of exercise-induced vascular benefits. We aim to investigate the involvement of peroxisome proliferator-activated receptor δ (PPARδ) in exercise-induced vascular functional improvement...
November 17, 2016: Diabetes
https://www.readbyqxmd.com/read/27854219/sil1-mutant-mice-elucidate-chaperone-function-in-neurological-disorders
#8
Stephan Buchkremer, José Andrés González Coraspe, Joachim Weis, Andreas Roos
Chaperone dysfunction leading to the build-up of misfolded proteins could frequently be linked to clinical manifestations also affecting the nervous system and the skeletal muscle. In addition, increase in chaperone function is beneficial to antagonize protein aggregation and thus represents a promising target for therapeutic concepts for many genetic and acquired chaperonopathies. However, little is known on the precise molecular mechanisms defining the cell and tissue abnormalities in the case of impaired chaperone function as well as on underlying effects in the case of compensatory up-regulation of chaperones...
May 27, 2016: Journal of Neuromuscular Diseases
https://www.readbyqxmd.com/read/27852331/energy-restriction-combined-with-dipeptidyl-peptidase-4-inhibitor-exerts-neuroprotection-in-obese-male-rats
#9
Hiranya Pintana, Pongpan Tanajak, Wasana Pratchayasakul, Piangkwan Sa-Nguanmoo, Titikorn Chunchai, Pattarapong Satjaritanun, Linlada Leelarphat, Nipon Chattipakorn, Siriporn C Chattipakorn
Dipeptidyl peptidase-4 (DDP-4) inhibitors and energy restriction (ER) are widely used to treat insulin resistance and type 2 diabetes mellitus. However, the effects of ER or the combination with vildagliptin on brain insulin sensitivity, brain mitochondrial function, hippocampal synaptic plasticity and cognitive function in obese insulin-resistant rats have never been investigated. We hypothesised that ER with DDP-4 inhibitor exerts better efficacy than ER alone in improving cognition in obese insulin-resistant male rats by restoring brain insulin sensitivity, brain mitochondrial function and hippocampal synaptic plasticity...
November 17, 2016: British Journal of Nutrition
https://www.readbyqxmd.com/read/27821438/akkermansia-muciniphila-improves-metabolic-profiles-by-reducing-inflammation-in-chow-diet-fed-mice
#10
Shaoqian Zhao, Wen Liu, Jiqiu Wang, Juan Shi, Yingkai Sun, Weiqing Wang, Guang Ning, Ruixin Liu, Jie Hong
Abnormal shifts in the composition of gut microbiota contribute to the pathogenesis of metabolic diseases, including obesity and type 2 diabetes (T2DM). The crosstalk between gut microbes and the host affects the inflammatory status and glucose tolerance of the individuals, but the underlying mechanisms have not been elucidated completely. In this study, we treated the lean chow diet-fed mice with Akkermansia muciniphila, which is thought to be inversely correlated with inflammation status and body weight in rodents and humans, and we found that A...
January 2017: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/27815317/macrophage-cyclooxygenase-2-protects-against-development-of-diabetic-nephropathy
#11
Xin Wang, Bing Yao, Yinqiu Wang, Xiaofeng Fan, Suwan Wang, Aolei Niu, Haichun Yang, Agnes Fogo, Ming-Zhi Zhang, Raymond C Harris
Diabetic nephropathy (DN) is characterized by increased macrophage infiltration, and proinflammatory "M1" macrophages contribute to development of DN. Previous studies by us and others have reported that macrophage cyclooxygenase-2 (COX-2) plays a role in polarization and maintenance of a macrophage tissue reparative "M2" phenotype. We examined the effects of macrophage COX-2 on development of DN in type I diabetes. Cultured macrophages with COX-2 deletion exhibited an "M1" phenotype, as demonstrated by higher iNOS and NF-κB levels but lower IL-4Rα levels...
November 4, 2016: Diabetes
https://www.readbyqxmd.com/read/27814504/inflammation-improves-glucose-homeostasis-through-ikk%C3%AE-xbp1s-interaction
#12
Junli Liu, Dorina Ibi, Koji Taniguchi, Jaemin Lee, Hilde Herrema, Bedia Akosman, Patrick Mucka, Mario Andres Salazar Hernandez, Muhemmet Fatih Uyar, Sang Won Park, Michael Karin, Umut Ozcan
It is widely believed that inflammation associated with obesity has an important role in the development of type 2 diabetes. IκB kinase beta (IKKβ) is a crucial kinase that responds to inflammatory stimuli such as tumor necrosis factor α (TNF-α) by initiating a variety of intracellular signaling cascades and is considered to be a key element in the inflammation-mediated development of insulin resistance. We show here, contrary to expectation, that IKKβ-mediated inflammation is a positive regulator of hepatic glucose homeostasis...
November 3, 2016: Cell
https://www.readbyqxmd.com/read/27813192/naltrexone-changes-the-expression-of-lipid-metabolism-related-proteins-in-the-endoplasmic-reticulum-er-stress-induced-hepatic-steatosis-in-mice
#13
Azam Moslehi, Fatemeh Nabavizadeh, Ali Zekri, Fatemeh Amiri
Endoplasmic reticulum (ER) stress is closely associated with several chronic diseases such as obesity, atherosclerosis, type 2 diabetes, and hepatic steatosis. Steatosis in hepatocytes may also lead to disorders such as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), fibrosis, and possibly cirrhosis. Opioid peptides are involved in triglyceride and cholesterol dysregulation. Naltrexone also attenuates ER stress induced hepatic steatosis in mice. In this study, we evaluated the effects of naltrexone on the expression of lipid metabolism-related nuclear factors and enzymes in the ER stress induced hepatic steatosis...
November 4, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27812542/activating-transcription-factor-4-promotes-mineralization-in-vascular-smooth-muscle-cells
#14
Masashi Masuda, Shinobu Miyazaki-Anzai, Audrey L Keenan, Yuji Shiozaki, Kayo Okamura, Wallace S Chick, Kristina Williams, Xiaoyun Zhao, Shaikh Mizanoor Rahman, Yin Tintut, Christopher M Adams, Makoto Miyazaki
Emerging evidence indicates that upregulation of the ER stress-induced pro-osteogenic transcription factor ATF4 plays an important role in vascular calcification, a common complication in patients with aging, diabetes, and chronic kidney disease (CKD). In this study, we demonstrated the pathophysiological role of ATF4 in vascular calcification using global Atf4 KO, smooth muscle cell-specific (SMC-specific) Atf4 KO, and transgenic (TG) mouse models. Reduced expression of ATF4 in global ATF4-haplodeficient and SMC-specific Atf4 KO mice reduced medial and atherosclerotic calcification under normal kidney and CKD conditions...
November 3, 2016: JCI Insight
https://www.readbyqxmd.com/read/27802439/metabolic-stress-induces-caspase-3-mediated-degradation-and-inactivation-of-farnesyl-and-geranylgeranyl-transferase-activities-in-pancreatic-%C3%AE-cells
#15
Rajakrishnan Veluthakal, Daleep K Arora, Marc L Goalstone, Renu A Kowluru, Anjaneyulu Kowluru
BACKGROUND/AIMS: At least 300 prenylated proteins are identified in the human genome; the majority of which partake in a variety of cellular processes including growth, differentiation, cytoskeletal organization/dynamics and vesicle trafficking. Aberrant prenylation of proteins is implicated in human pathologies including cancer; neurodegenerative diseases, retinitis pigmentosa, and premature ageing syndromes. Original observations from our laboratory have demonstrated that prenylation of proteins [small G-proteins and γ-subunits of trimeric G-proteins] is requisite for physiological insulin secretion...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27795806/c1q-tnf-related-protein-9-protects-diabetic-rat-heart-against-ischemia-reperfusion-injury-role-of-endoplasmic-reticulum-stress
#16
Sanxing Bai, Liang Cheng, Yang Yang, Chongxi Fan, Dajun Zhao, Zhigang Qin, Xiao Feng, Lin Zhao, Jipeng Ma, Xiaowu Wang, Jian Yang, Xuezeng Xu, Dinghua Yi, Wei Yi
As a newly identified adiponectin paralog, C1q/TNF-related protein 9 (CTRP9) reduces myocardial ischemia reperfusion (IR) injury through partially understood mechanisms. In the present study, we sought to identify the role of endoplasmic reticulum stress (ERS) in CTRP9 induced cardioprotection in diabetic heart. Isolated hearts from high-fat-diet (HFD) induced type 2 diabetic Sprague-Dawley rats were subjected to ex vivo IR protocol via a Langendorff apparatus at the presence of globular CTRP9. CTRP9 significantly improved post-IR heart function and reduced cardiac infarction, cardiomyocytes apoptosis, Caspase-3, Caspase-9, Caspase-12, TNF-α expression, and lactate dehydrogenase activity...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27794481/activated-protein-c-prevents-methylglyoxal-induced-endoplasmic-reticulum-stress-and-cardiomyocyte-apoptosis-via-regulation-of-the-amp-activated-protein-kinase-signaling-pathway
#17
Dae-Hwan Nam, Jung-Hwa Han, Suji Kim, YoungHyun Shin, Jae Hyang Lim, Hyoung Chul Choi, Chang-Hoon Woo
Previous epidemiological studies have shown that methylglyoxal (MGO) levels are highly regulated in diabetic cardiovascular diseases. We have also previously reported that MGO mediates ER stress and apoptosis in cardiomyocytes. Furthermore, activated protein C (APC) has recently been shown to play a protective role against ER stress, as well as a cardioprotective role against ischemia and reperfusion injury by augmenting the AMP-activated protein kinase (AMPK) signaling pathway. Therefore, we hypothesized that APC protects against MGO-induced cardiomyocyte apoptosis through the inhibition of ER stress...
October 26, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27793043/endoplasmic-reticulum-stress-induced-neuronal-inflammatory-response-and-apoptosis-likely-plays-a-key-role-in-the-development-of-diabetic-encephalopathy
#18
Zhouguang Wang, Yan Huang, Yi Cheng, Yi Tan, Fenzan Wu, Jiamin Wu, Hongxue Shi, Hongyu Zhang, Xichong Yu, Hongchang Gao, Li Lin, Jun Cai, Jinsan Zhang, Xiaokun Li, Lu Cai, Jian Xiao
We assumed that diabetic encephalopathy (DEP) may be induced by endoplasmic reticulum (ER)-mediated inflammation and apoptosis in central nervous system. To test this notion, here we investigated the neuronal ER stress and associated inflammation and apoptosis in a type 2 diabetes model induced with high-fat diet/streptozotocin in Sprague-Dawley rats. Elevated expressions of ER stress markers, including glucose-regulated protein 78 (GRP78), activating transcription factor-6 (ATF-6), X-box binding protein-1 (XBP-1), and C/EBP homologous protein, and phosphor-Jun N-terminal kinase (p-JNK) were evident in the hippocampus CA1 of diabetic rats...
October 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27779479/pronociceptive-effects-induced-by-cutaneous-application-of-a-transient-receptor-potential-ankyrin-1-trpa1-channel-agonist-methylglyoxal-in-diabetic-animals-comparison-with-tunicamycin-induced-endoplastic-reticulum-stress
#19
H Viisanen, H Chapman, H Wei, M Lasierra Losada, A Koivisto, K E Akerman, A Pertovaara
Methylglyoxal (MG) is a reactive carbonyl compound generated in diabetes mellitus. MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity. Here we studied whether exposure to diabetes and thereby to elevated endogenous MG modulates hypersensitivity induced by intradermal MG. Moreover, since diabetes induces endoplasmic reticulum (ER) stress, we compared the role of TRPA1 in diabetes and ER stress by assessing whether tunicamycin-induced ER stress, without diabetes, produces TRPA1-mediated pain hypersensitivity and by assessing whether ER stress and diabetes have similar modulatory effects on MG-induced hypersensitivity...
August 2016: Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society
https://www.readbyqxmd.com/read/27777138/effects-of-4-phenyl-butyric-acid-on-high-glucose-induced-alterations-in-dorsal-root-ganglion-neurons
#20
Dilip Sharma, Jitendra Narain Singh, Shyam S Sharma
Mechanisms and pathways involving in diabetic neuropathy are still not fully understood but can be unified by the process of overproduction of reactive oxygen species (ROS) such as superoxide, endoplasmic reticulum (ER) stress, downstream intracellular signaling pathways and their modulation. Susceptibility of dorsal root ganglion (DRG) to internal/external hyperglycemic environment stress contributes to the pathogenesis and progression of diabetic neuropathy. ER stress leads to abnormal ion channel function, gene expression, transcriptional regulation, metabolism and protein folding...
December 2, 2016: Neuroscience Letters
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