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er stress and diabetes

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https://www.readbyqxmd.com/read/28942246/inhibition-of-hepatocyte-nuclear-factor-1b-induces-hepatic-steatosis-through-dpp4-nox1-mediated-regulation-of-superoxide
#1
Zi Long, Meng Cao, Shuhao Su, Guangyuan Wu, Fansen Meng, Hao Wu, Jiangzheng Liu, Weihua Yu, Kamran Atabai, Xin Wang
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder that is closely associated with insulin resistance and type 2 diabetes. Previous studies have suggested that hepatocyte nuclear factor 1b (HNF1b) ameliorates insulin resistance. However, the role of HNF1b in the regulation of lipid metabolism and hepatic steatosis remains poorly understood. We found that HNF1b expression was decreased in steatotic livers. We injected mice with lentivirus (LV) expressing HNF1b shRNA to generate mice with hepatic knockdown of HNF1b...
September 20, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28939212/fortilin-a-potential-target-for-the-prevention-and-treatment-of-human-diseases
#2
Decha Pinkaew, Ken Fujise
Fortilin is a highly conserved 172-amino-acid polypeptide found in the cytosol, nucleus, mitochondria, extracellular space, and circulating blood. It is a multifunctional protein that protects cells against apoptosis, promotes cell growth and cell cycle progression, binds calcium (Ca(2+)) and has antipathogen activities. Its role in the pathogenesis of human and animal diseases is also diverse. Fortilin facilitates the development of atherosclerosis, contributes to both systemic and pulmonary arterial hypertension, participates in the development of cancers, and worsens diabetic nephropathy...
2017: Advances in Clinical Chemistry
https://www.readbyqxmd.com/read/28938442/angiotensin-ii-causes-beta-cell-dysfunction-through-an-er-stress-induced-pro-inflammatory-response
#3
Stanley M H Chan, Yeh-Siang Lau, Alyson A Miller, Jacqueline M Ku, Simon Potocnik, Ji-Ming Ye, Owen L Woodman, Terence P Herbert
The metabolic syndrome is associated with an increase in the activation of renin angiotensin system (RAS) and inhibition of RAS reduces the incidence of new onset diabetes. Importantly, angiotensin II (AngII), independently of its vasoconstrictor action causes beta-cell inflammation and dysfunction, which may be an early step in the development of type-2 diabetes. The aim of this study was to determine how AngII causes beta cell dysfunction. Islets of Langerhans were isolated from C57BL/6J mice that had been infused with AngII in the presence or absence of taurine-conjugated ursodeoxycholic acid (TUDCA) and effects on ER stress, inflammation and beta cell function determined...
August 17, 2017: Endocrinology
https://www.readbyqxmd.com/read/28930750/tauroursodeoxycholic-acid-reduces-arterial-stiffness-and-improves-endothelial-dysfunction-in-type-2-diabetic-mice
#4
Micah L Battson, Dustin M Lee, Dillon K Jarrell, Shoufei Hou, Kayl E Ecton, Anna B Phan, Christopher L Gentile
BACKGROUND/AIMS: Endoplasmic reticulum (ER) stress has emerged as a potential mechanism contributing to diabetes and its comorbidities. However, the importance of ER stress in diabetic vascular dysfunction is unclear. The purpose of this study was to examine the effects of the ER stress inhibitor, tauroursodeoxycholic acid (TUDCA), on arterial stiffness and endothelial dysfunction in type 2 diabetic mice. METHODS: Carotid and mesenteric artery endothelial function were assessed via ex vivo pressure myography, and arterial stiffness was measured by aortic pulse wave velocity...
September 21, 2017: Journal of Vascular Research
https://www.readbyqxmd.com/read/28928238/talk-1-channels-control-%C3%AE-cell-endoplasmic-reticulum-ca-2-homeostasis
#5
Nicholas C Vierra, Prasanna K Dadi, Sarah C Milian, Matthew T Dickerson, Kelli L Jordan, Patrick Gilon, David A Jacobson
Ca(2+) handling by the endoplasmic reticulum (ER) serves critical roles in controlling pancreatic β cell function and becomes perturbed during the pathogenesis of diabetes. ER Ca(2+) homeostasis is determined by ion movements across the ER membrane, including K(+) flux through K(+) channels. We demonstrated that K(+) flux through ER-localized TALK-1 channels facilitated Ca(2+) release from the ER in mouse and human β cells. We found that β cells from mice lacking TALK-1 exhibited reduced basal cytosolic Ca(2+) and increased ER Ca(2+) concentrations, suggesting reduced ER Ca(2+) leak...
September 19, 2017: Science Signaling
https://www.readbyqxmd.com/read/28923347/sulforaphane-improves-disrupted-er-mitochondria-interactions-and-suppresses-exaggerated-hepatic-glucose-production
#6
Emily Tubbs, Annika S Axelsson, Guillaume Vial, Claes B Wollheim, Jennifer Reuisset, Anders H Rosengren
AIMS: Exaggerated hepatic glucose production is one of the hallmarks of type 2 diabetes. Sulforaphane (SFN) has been suggested as a new potential anti-diabetic compound. However, the effects of SFN in hepatocytes are yet unclear. Accumulating evidence points to the close structural contacts between the ER and mitochondria, known as mitochondria-associated ER membranes (MAMs), as important hubs for hepatic metabolism. We wanted to investigate whether SFN could affect hepatic glucose production and MAMs...
September 16, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28901409/epigallocatechin%C3%A2-3%C3%A2-gallate-protects-from-high-glucose-induced-podocyte-apoptosis-via-suppressing-endoplasmic-reticulum-stress
#7
Chunhong Xiang, Xiaoyan Xiao, Bei Jiang, Mengkun Zhou, Yidan Zhang, Hui Li, Zhao Hu
Podocytes serve a critical role in the development of many glomerular diseases, including diabetic nephropathy (DN). Epigallocatechin‑3‑gallate (EGCG), a predominant polyphenolic component of green tea, has indicated its therapeutic effects in diabetes. In the present study, mouse podocyte cells were cultured in vitro, cell injury was induced by high glucose, and the protective effect of EGCG on cell proliferation and apoptosis and the underlying mechanisms were investigated. The results demonstrated that high glucose significantly inhibited cell proliferation after 48 and 72 h compared with normal glucose and mannitol treatment...
August 29, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28900935/metabolic-disorders-and-cancer-hepatocyte-store-operated-ca-2-channels-in-nonalcoholic-fatty-liver-disease
#8
Eunüs S Ali, Grigori Y Rychkov, Greg J Barritt
In steatotic hepatocytes, intracellular Ca(2+) homeostasis is substantially altered compared to normal. Decreased Ca(2+) in the endoplasmic reticulum (ER) can lead to ER stress, an important mediator of the progression of liver steatosis to nonalcoholic steatohepatitis, type 2 diabetes, and hepatocellular carcinoma. Store-operated Ca(2+) channels (SOCs) in hepatocytes are composed principally of Orai1 and STIM1 proteins. Their main role is the maintenance of adequate Ca(2+) in the lumen of the ER. In steatotic hepatocytes, store-operated Ca(2+) entry (SOCE) is substantially inhibited...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28888981/hypoxia-in-3t3-l1-adipocytes-suppresses-adiponectin-expression-via-the-perk-and-ire1-unfolded-protein-response
#9
Qian Guo, Sanli Jin, Hailong Hu, Ying Zhou, Yuheng Yan, He Zong, Yu Wang, Hongjuan He, Yuri Oh, Chuanpeng Liu, Ning Gu
Adiponectin, an adipocytokine produced by adipocytes, functions as an anti-inflammatory and anti-apoptotic substance, while also enhancing insulin sensitivity. Patients or model animals with obesity or diabetes typically present attenuated expression of adiponectin. Moreover, obesity and diabetes are often accompanied with hypoxia in adipose tissue, which may result in endoplasmic reticulum (ER) stress as well as low expression of adiponectin. The purpose of this study was to investigate the specific role of the unfolded protein response (UPR) involved in the low expression of adiponectin induced by hypoxia...
September 6, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28880478/role-of-g-proteins-in-islet-function-in-health-and-diabetes
#10
REVIEW
Anjaneyulu Kowluru
Glucose-stimulated insulin secretion (GSIS) involves interplay between metabolic and cationic events. Seminal contributions from multiple laboratories affirm essential roles for small G-proteins (Rac1, Cdc42, Arf6, Rab27A) in GSIS. Activation of these signalling proteins promotes cytoskeletal remodeling, transport and docking of insulin granules on the plasma membrane for exocytotic secretion of insulin. Evidence in rodent and human islets suggests key roles for lipidation (farnesylation and geranylgeranylation) of these G-proteins for their targeting to appropriate cellular compartments for optimal regulation of effectors leading to GSIS...
September 2017: Diabetes, Obesity & Metabolism
https://www.readbyqxmd.com/read/28867719/er-stress-and-disease-toward-prevention-and-treatment
#11
Masayuki Kaneko, Kazunori Imaizumi, Atsushi Saito, Soshi Kanemoto, Rie Asada, Koji Matsuhisa, Yosuke Ohtake
Secretory and membrane proteins are synthesized in ribosomes, then mature in the endoplasmic reticulum (ER), but if ER function is impaired, immature defective proteins accumulate in the ER. This situation is called ER stress: in response, a defensive mechanism called the unfolded protein response (UPR) is activated in cells to reduce the defective proteins. During the UPR, the ER transmembrane sensor molecules inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF6), and RNA-dependent protein kinase (PKR)-like ER kinase (PERK) are activated, stress signals are transduced to the outside of the ER, and various cell responses, including gene induction, occur...
2017: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28864287/age-related-cataracts-role-of-unfolded-protein-response-ca-2-mobilization-epigenetic-dna-modifications-and-loss-of-nrf2-keap1-dependent-cytoprotection
#12
REVIEW
Palsamy Periyasamy, Toshimichi Shinohara
Age-related cataracts are closely associated with lens chronological aging, oxidation, calcium imbalance, hydration and crystallin modifications. Accumulating evidence indicates that misfolded proteins are generated in the endoplasmic reticulum (ER) by most cataractogenic stresses. To eliminate misfolded proteins from cells before they can induce senescence, the cells activate a clean-up machinery called the ER stress/unfolded protein response (UPR). The UPR also activates the nuclear factor-erythroid-2-related factor 2 (Nrf2), a central transcriptional factor for cytoprotection against stress...
September 2017: Progress in Retinal and Eye Research
https://www.readbyqxmd.com/read/28839162/microrna-204-promotes-vascular-endoplasmic-reticulum-stress-and-endothelial-dysfunction-by-targeting-sirtuin1
#13
Modar Kassan, Ajit Vikram, Qiuxia Li, Young-Rae Kim, Santosh Kumar, Mohanad Gabani, Jing Liu, Julia S Jacobs, Kaikobad Irani
Endoplasmic reticulum (ER) stress has been implicated in vascular endothelial dysfunction of obesity, diabetes, and hypertension. MicroRNAs play an important role in regulating ER stress. Here we show that microRNA-204 (miR-204) promotes vascular ER stress and endothelial dysfunction by targeting the Sirtuin1 (Sirt1) lysine deacetylase. Pharmacologic ER stress induced by tunicamycin upregulates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cells in vitro. Inhibition of miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1...
August 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28835988/vldl-and-apolipoprotein-ciii-induce-er-stress-and-inflammation-and-attenuate-insulin-signalling-via-toll-like-receptor-2-in-mouse-skeletal-muscle-cells
#14
Gaia Botteri, Marta Montori, Anna Gumà, Javier Pizarro, Lídia Cedó, Joan Carles Escolà-Gil, Diana Li, Emma Barroso, Xavier Palomer, Alison B Kohan, Manuel Vázquez-Carrera
AIM/HYPOTHESIS: Here, our aim was to examine whether VLDL and apolipoprotein (apo) CIII induce endoplasmic reticulum (ER) stress, inflammation and insulin resistance in skeletal muscle. METHODS: Studies were conducted in mouse C2C12 myotubes, isolated skeletal muscle and skeletal muscle from transgenic mice overexpressing apoCIII. RESULTS: C2C12 myotubes exposed to VLDL showed increased levels of ER stress and inflammatory markers whereas peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and AMP-activated protein kinase (AMPK) levels were reduced and the insulin signalling pathway was attenuated...
August 23, 2017: Diabetologia
https://www.readbyqxmd.com/read/28827061/disruption-of-the-mitochondria-associated-er-membrane-mam-plays-a-central-role-in-palmitic-acid-induced-insulin-resistance
#15
Satoko Shinjo, Shuying Jiang, Masaaki Nameta, Tomohiro Suzuki, Mai Kanai, Yuta Nomura, Nobuhito Goda
The mitochondria-associated ER membrane (MAM) is a specialized subdomain of ER that physically connects with mitochondria. Although disruption of inter-organellar crosstalk via the MAM impairs cellular homeostasis, its pathological significance in insulin resistance in type 2 diabetes mellitus remains unclear. Here, we reveal the importance of reduced MAM formation in the induction of fatty acid-evoked insulin resistance in hepatocytes. Palmitic acid (PA) repressed insulin-stimulated Akt phosphorylation in HepG2 cells within 12hours...
August 4, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28826228/carbon-monoxide-inhibits-islet-apoptosis-via-induction-of-autophagy
#16
Do-Sung Kim, Lili Song, Jingjing Wang, Hongju Wu, Wenyu Gou, Wanxing Cui, Jae-Sung Kim, Hongjun Wang
AIM: Carbon monoxide (CO) functions as a therapeutic molecule in various disease models because of its anti-inflammatory and anti-apoptotic properties. We investigated the capacity of CO to reduce hypoxia-induced islet cell death and dysfunction in human and mouse models. RESULTS: Culturing islets in CO-saturated medium protected them from hypoxia-induced apoptosis, and preserved β cell function by suppressing expression of pro-apoptotic (Bim, PARP, Cas-3), pro-inflammatory (TNF-α), and ER stress (glucose-regulated protein 94, grp94, CHOP) proteins...
August 21, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28815530/role-of-endoplasmic-reticulum-mitochondria-communication-in-type-2-diabetes
#17
Jennifer Rieusset
Although mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and disrupted lipid and calcium (Ca(2+)) homeostasis are classically associated with both insulin resistance and β-cell dysfunction in type 2 diabetes mellitus (T2DM), the interplay between these metabolic stresses is less known. Both organelles interact through contact points known as mitochondria-associated membranes (MAM), in order to exchange both lipids and Ca(2+) and regulate cellular homeostasis. Recent evidences suggest that MAM could be an important hub for hormonal and nutrient signaling in the liver and that ER-mitochondria miscommunication could participate to hepatic insulin resistance, highlighting the importance of MAM in the control of glucose homeostasis...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28797256/selenoprotein-s-a-therapeutic-target-for-diabetes-and-macroangiopathy
#18
REVIEW
Shan-Shan Yu, Jian-Ling Du
Inflammatory response, oxidative stress, and endoplasmic reticulum (ER) stress are important pathophysiological bases of the occurrence and development of diabetes mellitus (DM) and macroangiopathy complications. Selenoprotein S (SELENOS) is involved in the regulation of these mechanisms; therefore, its association with DM and macroangiopathy has gradually received attention from scholars worldwide. SELENOS has different biological functions in different tissues and organs: it exerts antioxidant protection and has anti-ER stress effects in the pancreas and blood vessels, while it promotes the occurrence and development of insulin resistance in the liver, adipose tissue, and skeletal muscle...
August 10, 2017: Cardiovascular Diabetology
https://www.readbyqxmd.com/read/28794417/inhibition-of-endoplasmic-reticulum-stress-preserves-the-integrity-of-blood-spinal-cord-barrier-in-diabetic-rats-subjected-to-spinal-cord-injury
#19
Zili He, Shuang Zou, Jiayu Yin, Zhengzheng Gao, Yanlong Liu, Yanqing Wu, Huacheng He, Yulong Zhou, Qingqing Wang, Jiawei Li, Fenzan Wu, Hua-Zi Xu, Xiaofeng Jia, Jian Xiao
The blood-spinal cord barrier (BSCB) plays significance roles in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) impairs endothelial cell function and integrity of BSCS. Endoplasmic reticulum (ER) stress occurs in the early stages of SCI and affects prognosis and cell survival. However, the relationship between ER stress and the integrity of BSCB in diabetic rats after SCI remains unclear. Here we observed that diabetic rats showed increased extravasation of Evans Blue (EB) dye, and loss of endothelial cells and pericytes 1 day after SCI compared to non-diabetic rats...
August 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28782427/berberine-improves-diabetic-encephalopathy-through-the-sirt1-er-stress-pathway-in-db-db-mice
#20
Hong-Ying Li, Xin-Chen Wang, Yu-Min Xu, Na-Chuan Luo, Si Luo, Xu-Yi Hao, Shu-Yi Cheng, Jian-Song Fang, Qi Wang, Shi-Jie Zhang, Yun-Bo Chen
The association between diabetes and dementia has been well demonstrated by epidemiologic studies. Berberine (BBR) has been reported to ameliorate diabetes and diabetic encephalopathy (DE). However, the mechanism is still unknown. In this study, we employ a diabetic model, db/db mice, to explore whether BBR could protect DE through the SIRT1/endoplasmic reticulum (ER) stress pathway. Behavioral results (Morris water maze, Y-maze spontaneous alternation test, and fear conditioning test) showed that oral administration of BBR (50 mg/kg) improved the learning and memory ability...
September 21, 2017: Rejuvenation Research
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