keyword
MENU ▼
Read by QxMD icon Read
search

AKT AND pancreatic beta cells

keyword
https://www.readbyqxmd.com/read/27816562/over-expression-of-insulin-response-element-binding-protein-1-ire-bp1-in-mouse-pancreatic-islets-increases-expression-of-rack1-and-tctpp-beta-cell-markers-of-high-glucose-sensitivity
#1
Betty C Villafuerte, Michelle T Barati, Madhavi J Rane, Susan Isaacs, Ming Li, Daniel W Wilkey, Michael L Merchant
BACKGROUND: A targeted analysis of the 50kDa C-terminal fragment of insulin-response element binding protein-1 (IRE-BP1) activation of target genes through the insulin receptor substrate receptor/PI-3 kinase/Akt pathway has been demonstrated for the insulin growth factor-1 receptor. The broader effects of 50kDa C-terminal IRE-BP1 fragment over-expression on protein abundance in pancreatic islet beta cells have not been determined. RESULTS: Liquid-chromatography coupled to tandem mass spectrometry (LC-MS/MS) analyses of replicate lysates of pancreatic islets isolated from background strain animals and transgenic animals, overexpressing IRE-BP1 in pancreatic islet beta cells, demonstrated statistically significant increases in the expression of proteins involved in protein synthesis, endoplasmic reticulum (ER) stress and scaffolding proteins important for protein kinase C signaling; some of which were confirmed by immunoblot analyses...
November 3, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27717730/l-arginine-supplementation-improves-insulin-sensitivity-and-beta-cell-function-in-the-offspring-of-diabetic-rats-through-akt-and-pdx-1-activation
#2
Diego Soares Carvalho, Marilia Melo Diniz, André Abour Haidar, Maria de Fátima Cavanal, Eduardo da Silva Alves, Angelo Rafael Carpinelli, Frida Zaladek Gil, Aparecida Emiko Hirata
Maternal hyperglycemia can result in defects in glucose metabolism and pancreatic β-cell function in offspring. The purpose of this study was to evaluate the impact of maternal diabetes mellitus on pancreatic islets, muscle and adipose tissue of the offspring, with or without oral l-Arginine supplementation. The induction of diabetes was performed using streptozotocin (60mg/kg). Animals were studied at 3 months of age and treatment (sucrose or l-Arginine) was administered from weaning. We observed that l-Arg improved insulin sensitivity in the offspring of diabetic mothers (DA), reflected by higher insulin-induced phosphorylation of Akt in muscle and adipose tissue...
October 4, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27609771/insulin-promotes-proliferation-and-fibrosing-responses-in-activated-pancreatic-stellate-cells
#3
Jiayue Yang, Richard T Waldron, Hsin-Yuan Su, Aune Moro, Hui-Hua Chang, Guido Eibl, Kevin Ferreri, Fouad R Kandeel, Aurelia Lugea, Ling Li, Stephen J Pandol
Epidemiological studies support strong links between obesity, diabetes, and pancreatic disorders including pancreatitis and pancreatic adenocarcinoma (PDAC). Type 2 diabetes (T2DM) is associated with insulin resistance, hyperglycemia, and hyperinsulinemia, the latter due to increased insulin secretion by pancreatic beta-cells. We reported that high-fat diet-induced PDAC progression in mice is associated with hyperglycemia, hyperinsulinemia, and activation of pancreatic stellate cells (PaSC). We investigated here the effects of high concentrations of insulin and glucose on mouse and human PaSC growth and fibrosing responses...
October 1, 2016: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://www.readbyqxmd.com/read/27568466/microrna-17-92-cluster-regulates-pancreatic-beta-cell-proliferation-and-adaptation
#4
Yaxi Chen, Li Tian, Shan Wan, Ying Xie, Xiang Chen, Xiao Ji, Qian Zhao, Chunyu Wang, Kun Zhang, Janet M Hock, Haoming Tian, Xijie Yu
MiR-17-92 cluster contributes to the regulation of mammalian development, aging and tumorigenesis. The functional roles of miR-17-92 in pancreatic beta-cells are largely unknown. In this study, we found that conditional deletion of miR-17-92 in mouse pancreatic beta-cells (miR-17-92βKO) significantly reduces glucose tolerance and the first phase of insulin secretion, despite normal ad libitum fed and fasting glucose levels. Proliferation is down-regulated in pancreatic beta-cells after deleting miR-17-92. MiR-17-92βKO mice show higher phosphatase and tensin homologue (PTEN) and lower phosphorylated AKT in islets...
December 5, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27531748/hypoxia-and-transforming-growth-factor-%C3%AE-cooperate-to-induce-fibulin-5-expression-in-pancreatic-cancer
#5
Mary Topalovski, Michelle Hagopian, Miao Wang, Rolf A Brekken
The deposition of extracellular matrix (ECM) is a defining feature of pancreatic ductal adenocarcinoma (PDA), where ECM signaling can promote cancer cell survival and epithelial plasticity programs. However, ECM signaling can also limit PDA tumor growth by producing cytotoxic levels of reactive oxygen species. For example, excess fibronectin stimulation of α5β1 integrin on stromal cells in PDA results in reduced angiogenesis and increased tumor cell apoptosis because of oxidative stress. Fibulin-5 (Fbln5) is a matricellular protein that blocks fibronectin-integrin interaction and thus directly limits ECM-driven reactive oxygen species production and supports PDA progression...
October 14, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27408772/pi3-kinases-p110%C3%AE-and-pi3k-c2%C3%AE-negatively-regulate-camp-via-pde3-8-to-control-insulin-secretion-in-mouse-and-human-islets
#6
Jelena Kolic, Jocelyn E Manning Fox, Oleg G Chepurny, Aliya F Spigelman, Mourad Ferdaoussi, Frank Schwede, George G Holz, Patrick E MacDonald
OBJECTIVES: Phosphatidylinositol-3-OH kinase (PI3K) signalling in the endocrine pancreas contributes to glycaemic control. However, the mechanism by which PI3K modulates insulin secretion from the pancreatic beta cell is poorly understood. Thus, our objective was two-fold; to determine the signalling pathway by which acute PI3K inhibition enhances glucose-stimulated insulin secretion (GSIS) and to examine the role of this pathway in islets from type-2 diabetic (T2D) donors. METHODS: Isolated islets from mice and non-diabetic or T2D human donors, or INS 832/13 cells, were treated with inhibitors of PI3K and/or phosphodiesterases (PDEs)...
July 2016: Molecular Metabolism
https://www.readbyqxmd.com/read/27155954/the-insulin-signaling-pathway-of-the-pancreatic-islet-is-impaired-in-adult-mice-offspring-of-mothers-fed-a-high-fat-diet
#7
Isabele Bringhenti, Fernanda Ornellas, Carlos Alberto Mandarim-de-Lacerda, Marcia Barbosa Aguila
OBJECTIVE: Mothers fed a high-fat (HF) diet can cause different adverse alterations in their offspring. The study aimed to verify the pancreatic islet structure and insulin-signaling pathway in adulthood of offspring of mothers fed a HF diet during the pregnancy. METHODS: Female mice (mothers) were randomly assigned to receive either standard chow (Mo-SC) or a HF diet (Mo-HF) ad libitum. After 2 mo on the experimental diets, 3-mo-old female mice were mated with male C57 BL/6 mice that were fed a SC diet...
October 2016: Nutrition
https://www.readbyqxmd.com/read/27110488/inter-domain-tagging-implicates-caveolin-1-in-insulin-receptor-trafficking-and-erk-signaling-bias-in-pancreatic-beta-cells
#8
Tobias Boothe, Gareth E Lim, Haoning Cen, Søs Skovsø, Micah Piske, Shu Nan Li, Ivan R Nabi, Patrick Gilon, James D Johnson
OBJECTIVE: The role and mechanisms of insulin receptor internalization remain incompletely understood. Previous trafficking studies of insulin receptors involved fluorescent protein tagging at their termini, manipulations that may be expected to result in dysfunctional receptors. Our objective was to determine the trafficking route and molecular mechanisms of functional tagged insulin receptors and endogenous insulin receptors in pancreatic beta-cells. METHODS: We generated functional insulin receptors tagged with pH-resistant fluorescent proteins between domains...
May 2016: Molecular Metabolism
https://www.readbyqxmd.com/read/27095850/secretagogin-affects-insulin-secretion-in-pancreatic-%C3%AE-cells-by-regulating-actin-dynamics-and-focal-adhesion
#9
Seo-Yun Yang, Jae-Jin Lee, Jin-Hee Lee, Kyungeun Lee, Seung Hoon Oh, Yu-Mi Lim, Myung-Shik Lee, Kong-Joo Lee
Secretagogin (SCGN), a Ca(2+)-binding protein having six EF-hands, is selectively expressed in pancreatic β-cells and neuroendocrine cells. Previous studies suggested that SCGN enhances insulin secretion by functioning as a Ca(2+)-sensor protein, but the underlying mechanism has not been elucidated. The present study explored the mechanism by which SCGN enhances glucose-induced insulin secretion in NIT-1 insulinoma cells. To determine whether SCGN influences the first or second phase of insulin secretion, we examined how SCGN affects the kinetics of insulin secretion in NIT-1 cells...
June 15, 2016: Biochemical Journal
https://www.readbyqxmd.com/read/27035653/long-term-exposure-of-pancreatic-%C3%AE-cells-to-palmitate-results-in-srebp-1c-dependent-decreases-in-glp-1-receptor-signaling-via-creb-and-akt-and-insulin-secretory-response
#10
Annalisa Natalicchio, Giuseppina Biondi, Nicola Marrano, Rossella Labarbuta, Federica Tortosa, Rosaria Spagnuolo, Rossella D'Oria, Emanuele Carchia, Anna Leonardini, Angelo Cignarelli, Sebastio Perrini, Luigi Laviola, Francesco Giorgino
The effects of prolonged exposure of pancreatic β-cells to high saturated fatty acids on glucagon-like peptide-1 (GLP-1) action were investigated. Murine islets, human pancreatic 1.1B4 cells, and rat INS-1E cells were exposed to palmitate for 24 hours. mRNA and protein expression/phosphorylation were measured by real-time RT-PCR and immunoblotting, respectively. Specific short interfering RNAs were used to knockdown expression of the GLP-1 receptor (Glp1r) and Srebf1. Insulin release was assessed with a specific ELISA...
June 2016: Endocrinology
https://www.readbyqxmd.com/read/27014088/beneficial-renal-and-pancreatic-phenotypes-in-a-mouse-deficient-in-fxyd2-regulatory-subunit-of-na-k-atpase
#11
REVIEW
Elena Arystarkhova
The fundamental role of Na,K-ATPase in eukaryotic cells calls for complex and efficient regulation of its activity. Besides alterations in gene expression and trafficking, kinetic properties of the pump are modulated by reversible association with single span membrane proteins, the FXYDs. Seven members of the family are expressed in a tissue-specific manner, affecting pump kinetics in all possible permutations. This mini-review focuses on functional properties of FXYD2 studied in transfected cells, and on noteworthy and unexpected phenotypes discovered in a Fxyd2 (-∕-) mouse...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/26983645/anti-diabetic-effect-of-3-hydroxy-2-naphthoic-acid-an-endoplasmic-reticulum-stress-reducing-chemical-chaperone
#12
Sun-mi Park, Jungsook Choi, Tae-gyu Nam, Jin-mo Ku, Kwiwan Jeong
Lots of experimental and clinical evidences indicate that chronic exposure to saturated fatty acids and high level of glucose is implicated in insulin resistance, beta cell failure and ultimately type 2 diabetes. In this study, we set up cell-based experimental conditions to induce endoplasmic reticulum (ER) stress and insulin resistance using high concentration of palmitate (PA). Hydroxynaphthoic acids (HNAs) were formerly identified as novel chemical chaperones to resolve ER stress induced by tunicamycin...
May 15, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/26868297/pkc%C3%AE-is-essential-for-pancreatic-%C3%AE-cell-replication-during-insulin-resistance-by-regulating-mtor-and-cyclin-d2
#13
Jayalakshmi Lakshmipathi, Juan Carlos Alvarez-Perez, Carolina Rosselot, Gabriella P Casinelli, Rachel E Stamateris, Francisco Rausell-Palamos, Christopher P O'Donnell, Rupangi C Vasavada, Donald K Scott, Laura C Alonso, Adolfo Garcia-Ocaña
Adaptive β-cell replication occurs in response to increased metabolic demand during insulin resistance. The intracellular mediators of this compensatory response are poorly defined and their identification could provide significant targets for β-cell regeneration therapies. Here we show that glucose and insulin in vitro and insulin resistance in vivo activate protein kinase C ζ (PKCζ) in pancreatic islets and β-cells. PKCζ is required for glucose- and glucokinase activator-induced proliferation of rodent and human β-cells in vitro...
May 2016: Diabetes
https://www.readbyqxmd.com/read/26663079/npas4-transcription-factor-expression-is-regulated-by-calcium-signaling-pathways-and-prevents-tacrolimus-induced-cytotoxicity-in-pancreatic-beta-cells
#14
Thilo Speckmann, Paul V Sabatini, Cuilan Nian, Riley G Smith, Francis C Lynn
Cytosolic calcium influx activates signaling pathways known to support pancreatic beta cell function and survival by modulating gene expression. Impaired calcium signaling leads to decreased beta cell mass and diabetes. To appreciate the causes of these cytotoxic perturbations, a more detailed understanding of the relevant signaling pathways and their respective gene targets is required. In this study, we examined the calcium-induced expression of the cytoprotective beta cell transcription factor Npas4. Pharmacological inhibition implicated the calcineurin, Akt/protein kinase B, and Ca(2+)/calmodulin-dependent protein kinase signaling pathways in the regulation of Npas4 transcription and translation...
February 5, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/26446269/adverse-effects-of-vitamin-d-deficiency-on-the-pi3k-akt-pathway-and-pancreatic-islet-morphology-in-diet-induced-obese-mice
#15
Celina Carvalho Borges, Andreza Fernandes Salles, Isabele Bringhenti, Vanessa Souza-Mello, Carlos Alberto Mandarim-de-Lacerda, Marcia Barbosa Aguila
SCOPE: To investigate the impact of vitamin D deficiency on insulin resistance and abnormal glucose homeostasis in obesity. METHODS AND RESULTS: Sixty male C57BL/6 mice (3 months old) were fed a control diet (C-10% energy as fat) or a high-fat diet (HF-50% energy as fat), with or without vitamin D, for 8 weeks. There was no difference in body mass between the HF and HF/VitD- groups. Vitamin D deficiency (VitD) in the diet-induced obese mice increased hyperinsulinemia (p = 0...
February 2016: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/26279445/eruberin-a-a-natural-flavanol-glycoside-exerts-anti-fibrotic-action-on-pancreatic-stellate-cells
#16
Siu Wai Tsang, Hong-Jie Zhang, Ye-Gao Chen, Kathy Ka-Wai Auyeung, Zhao-Xiang Bian
BACKGROUND: Eruberin A (2, 3-dehydroflavonoid), a flavanol glycoside isolated from Pronephrium penangianum, has been used as a blood-nourishing folk medicine for centuries; however, it indeed possesses a variety of other health-promoting benefits including anti-fibrotic bioactivity. Activation of pancreatic stellate cells (PSCs) is the key initiating step in pancreatic fibrosis, which is a characteristic feature associated with chronic pancreatitis and pancreatic adenocarcinoma. METHODS: The anti-fibrotic effect of eruberin A and the underlying mechanisms of its anti-fibrotic action in LTC-14 cells, which retained essential characteristics and morphological features of primary PSCs, were examined by means of real-time polymerase chain reactions, Western blotting and immunostaining...
2015: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/26221611/effects-of-high-glucose-levels-and-glycated-serum-on-gip-responsiveness-in-the-pancreatic-beta-cell-line-hit-t15
#17
Alessandra Puddu, Roberta Sanguineti, Fabrizio Montecucco, Giorgio Luciano Viviani
Glucose-dependent insulinotropic peptide (GIP) is an incretin hormone produced in the gastrointestinal tract that stimulates glucose dependent insulin secretion. Impaired incretin response has been documented in diabetic patients and was mainly related to the inability of the pancreatic beta cells to secrete insulin in response to GIP. Advanced Glycation End Products (AGEs) have been shown to play an important role in pancreatic beta cell dysfunction. The aim of this study is to investigate whether the exposure to AGEs can induce GIP resistance in the pancreatic beta cell line HIT-T15...
2015: Journal of Diabetes Research
https://www.readbyqxmd.com/read/26131124/systematic-investigation-into-the-role-of-intermittent-high-glucose-in-pancreatic-beta-cells
#18
Chen Shao, Jianqiu Gu, Xin Meng, Hongzhi Zheng, Difei Wang
OBJECTIVES: Glucose fluctuation is suggested to be the leading cause of beta-cell damages. To determine how it induces beta-cell dysfunction, we systematically evaluated the effects of intermittent high glucose (IHG) in INS-1 rat pancreatic beta-cells on their proliferation activity, apoptosis, insulin secretion, reactive oxygen species (ROS), intracellular concentration of Ca(2+) ([Ca(2+)]i), and the PTEN expression as well as AKT phosphorylation. METHODS: Prior to the examinations, INS-1 cells were treated with normal glucose (NG, 11...
2015: International Journal of Clinical and Experimental Medicine
https://www.readbyqxmd.com/read/26099856/prolactin-stimulated-survivin-induction-is-required-for-beta-cell-mass-expansion-during-pregnancy-in-mice
#19
Yili Xu, Xiaojing Wang, Li Gao, Jiayu Zhu, Hui Zhang, Houxia Shi, Minna Woo, Xiaohong Wu
AIMS/HYPOTHESIS: Prolactin (PRL)-stimulated beta cell proliferation is critical for maternal pancreatic beta cell mass expansion during pregnancy. However, the molecular effectors of the multiple putative signalling pathways downstream of the PRL receptor (PRL-R) are still elusive. Survivin has been shown to be induced during pregnancy. The aim of the present study was to define the essential role of survivin in gestational beta cell mass expansion. METHODS: Expression of survivin was assessed in mouse islets during pregnancy and in insulinoma cells (INS-1) stimulated with PRL...
September 2015: Diabetologia
https://www.readbyqxmd.com/read/25950476/geniposide-promotes-beta-cell-regeneration-and-survival-through-regulating-%C3%AE-catenin-tcf7l2-pathway
#20
D D Yao, L Yang, Y Wang, C Liu, Y J Wei, X B Jia, W Yin, L Shu
T-cell factor 7-like 2 (TCF7L2) is an important transcription factor of Wnt/β-catenin signaling, which has critical roles in β-cell survival and regeneration. In preliminary screening assay, we found geniposide, a naturally occurring compound, was able to increase TCF7L2 mRNA level in Min6 cells. Here we aimed to investigate the role of geniposide in β-cell and underlying mechanism involved. Geniposide was found to promote β-cell survival by increasing β-cell proliferation and decreasing β-cell apoptosis in cultured mouse islets after challenge with diabetic stimuli...
2015: Cell Death & Disease
keyword
keyword
74060
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"