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Diabetes

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https://www.readbyqxmd.com/read/29449307/rage-deletion-confers-renoprotection-by-reducing-responsiveness-to-transforming-growth-factor-%C3%AE-and-increasing-resistance-to-apoptosis
#1
Shinji Hagiwara, Karly Sourris, Mark Ziemann, Wu Tieqiao, Muthukumar Mohan, Aaron D McClelland, Eoin Brennan, Josephine Forbes, Melinda Coughlan, Brooke Harcourt, Sally Penfold, Bo Wang, Gavin Higgins, Raelene Pickering, Assam El-Osta, Merlin C Thomas, Mark E Cooper, Phillip Kantharidis
Signalling via the receptor of advanced glycation end-products (RAGE) although complex and not fully elucidated in the setting of diabetes, is considered a key injurious pathway in the development of diabetic nephropathy (DN). We report here that RAGE deletion resulted in increased expression of fibrotic (collagen I and IV, fibronectin) and the inflammatory marker, MCP-1 in primary mouse mesangial cells (MC) and in kidney cortex. RNA-seq analysis in MCs from RAGE -/- and wild type mice confirmed these observations...
February 15, 2018: Diabetes
https://www.readbyqxmd.com/read/29444892/role-of-protein-phosphatase-1-and-inhibitor-of-protein-phosphatase-1-in-nitric-oxide-dependent-inhibition-of-the-dna-damage-response-in-pancreatic-%C3%AE-cells
#2
Bryndon J Oleson, Aaron Naatz, Sarah C Proudfoot, Chay Teng Yeo, John A Corbett
Nitric oxide is produced at micromolar levels by pancreatic β-cells during exposure to proinflammatory cytokines. While classically viewed as damaging, nitric oxide also activates pathways that promote β-cell survival. We have shown that nitric oxide, in a cell type selective manner, inhibits the DNA damage response (DDR) and, in doing so, protects β-cells from DNA damage-induced apoptosis. This study explores potential mechanisms by which nitric oxide inhibits DDR signaling. We show that inhibition of DDR signaling (measured by γH2AX formation and the phosphorylation of KAP1) is selective for nitric oxide, as other forms of reactive oxygen/nitrogen species do not impair DDR signaling...
February 14, 2018: Diabetes
https://www.readbyqxmd.com/read/29444891/metabolic-syndrome-is-associated-with-impaired-diastolic-function-independently-of-mri-derived-myocardial-extracellular-volume-the-mesa-study
#3
Ricardo Ladeiras-Lopes, Henrique T Moreira, Nuno Bettencourt, Ricardo Fontes-Carvalho, Francisco Sampaio, Bharath Ambale-Venkatesh, Colin Wu, Kiang Liu, Alain G Bertoni, Pamela Ouyang, David A Bluemke, João A Lima
The relationship of MetS (metabolic syndrome) and insulin resistance (one of its key pathophysiological mediators) with diastolic dysfunction and myocardial fibrosis is not well understood. This study aimed to evaluate the association of MetS with diastolic function and myocardial extracellular matrix (ECM) using cardiac magnetic resonance imaging (CMR) in a large community-based population.This cross-sectional analysis included 1,582 participants from the Multi-Ethnic Study of Atherosclerosis with left ventricular ejection fraction ≥50% and no past history of cardiac events...
February 14, 2018: Diabetes
https://www.readbyqxmd.com/read/29440067/perilipin-3-deficiency-stimulates-thermogenic-beige-adipocytes-through-ppar%C3%AE-activation
#4
Yun Kyung Lee, Jee Hyung Sohn, Ji Seul Han, Yoon Jeong Park, Yong Geun Jeon, Yul Ji, Knut Tomas Dalen, Carole Sztalryd, Alan R Kimmel, Jae Bum Kim
Beige adipocytes can dissipate energy as heat. Elaborate communication between metabolism and gene expression is important in the regulation of beige adipocytes. While lipid droplet (LD)-binding proteins play important roles in adipose tissue biology, it remains unknown whether perilipin 3 ( Plin3 ) is involved in the regulation of beige adipocyte formation and thermogenic activities. Here, we demonstrate that Plin3 ablation stimulates beige adipocytes and thermogenic gene expression in inguinal white adipose tissue (iWAT)...
February 13, 2018: Diabetes
https://www.readbyqxmd.com/read/29440278/regulation-of-k-atp-channel-trafficking-in-pancreatic-%C3%AE-cells-by-protein-histidine-phosphorylation
#5
Shekhar Srivastava, Zhai Li, Irfana Soomro, Ying Sun, Jianhui Wang, Li Bao, William A Coetzee, Charles A Stanley, Chonghong Li, Edward Y Skolnik
Protein histidine phosphatase 1 (PHPT-1) is an evolutionarily conserved 14 kDa protein that dephosphorylates phosphohistidine. PHPT-1 -/- mice were generated to gain insight into the role of PHPT-1 and histidine phosphorylation/dephosphorylation in mammalian biology. PHPT-1 -/- mice exhibited neonatal hyperinsulinemic hypoglycemia due to impaired trafficking of KATPchannels to the plasma membrane in pancreatic β cells in response to low glucose and leptin and resembled patients with congenital hyperinsulinism (CHI)...
February 12, 2018: Diabetes
https://www.readbyqxmd.com/read/29436377/elevated-medium-chain-acylcarnitines-are-associated-with-gestational-diabetes-and-early-progression-to-type-2-diabetes-and-induce-pancreatic-%C3%AE-cell-dysfunction
#6
Battsetseg Batchuluun, Dana Al Rijjal, Kacey J Prentice, Judith A Eversley, Elena Burdett, Haneesha Mohan, Alpana Bhattacharjee, Erica P Gunderson, Ying Liu, Michael B Wheeler
Specific circulating metabolites have emerged as important risk factors for the development of diabetes. The acylcarnitines (acylCs) are a family of metabolites known to be elevated in type-2 diabetes (T2D) and linked to peripheral insulin resistance. However, the impact of AcylCs on pancreatic β-cell function is not well understood. Here, we profiled circulating acylCs in two diabetes cohorts: 1) women with gestational diabetes (GDM) and 2) women with recent GDM who later developed impaired glucose tolerance (IGT), new-onset T2D or returned to normoglycemia within a two-year follow-up period...
February 7, 2018: Diabetes
https://www.readbyqxmd.com/read/29432124/cdkn2a-b-t2d-gwas-risk-snps-impact-locus-gene-expression-and-proliferation-in-human-islets
#7
Yahui Kong, Rohit B Sharma, Socheata Ly, Rachel E Stamateris, William M Jesdale, Laura C Alonso
Genome-wide association studies link the CDKN2A/B locus with T2D risk, but mechanisms increasing risk remain unknown. The CDKN2A/B locus encodes cell cycle inhibitors p14, p15, and p16, MTAP, and ANRIL, a lncRNA. The goal of this study was to determine whether CDKN2A/B T2D risk-SNPs impact locus gene expression, insulin secretion, or beta cell proliferation, in human islets. Islets from non-diabetic donors (n=95) were tested for SNP genotype (rs10811661, rs2383208, rs564398, rs10757283), gene expression (p14, p15, p16, MTAP, ANRIL, PCNA, KI67, CCND2), insulin secretion (n=61) and beta cell proliferation (n=47)...
February 6, 2018: Diabetes
https://www.readbyqxmd.com/read/29432123/catestatin-inhibits-obesity-induced-macrophage-infiltration-and-inflammation-in-the-liver-and-suppresses-hepatic-glucose-production-leading-to-improved-insulin-sensitivity
#8
Wei Ying, Sumana Mahata, Gautam K Bandyopadhyay, Zhenqi Zhou, Joshua Wollam, Jessica Vu, Rafael Mayoral, Nai-Wen Chi, Nicholas J G Webster, Angelo Corti, Sushil K Mahata
The activation of Kupffer cells (KCs) and monocyte (Mc)-derived recruited macrophages (McMΦs) in the liver contributes to obesity-induced insulin resistance and type 2 diabetes. Diet-induced obese (DIO) mice treated with Chromogranin A (CgA) peptide catestatin (CST) showed several positive results. These included decreased hepatic/plasma lipids and plasma insulin, diminished expression of gluconeogenic genes, attenuated expression of pro-inflammatory genes, increased expression of anti-inflammatory genes in McMΦs, and inhibition of the infiltration of McMΦs resulting in improvement of insulin sensitivity...
February 6, 2018: Diabetes
https://www.readbyqxmd.com/read/29386225/pdgf-bb-carried-by-endothelial-cell-derived-extracellular-vesicles-reduces-vascular-smooth-muscle-cell-apoptosis-in-diabetes
#9
Gabriele Togliatto, Patrizia Dentelli, Arturo Rosso, Giusy Lombardo, Maddalena Gili, Sara Gallo, Chiara Gai, Anna Solini, Giovanni Camussi, Maria Felice Brizzi
Endothelial cell-derived extracellular vesicles (CD31EVs) are a new entity for therapeutic/prognostic purposes. The roles of CD31EVs as mediators of smooth muscle cell (VSMC) dysfunction in type 2 diabetes (T2D) is investigated herein.We demonstrated that, unlike non-diabetic, diabetic serum-derived-EVs (D-CD31EVs) boosted apoptosis resistance of VSMCs cultured in hyperglycaemic condition. Biochemical analysis revealed that this effect relies on changes in the balance between anti-apoptotic/pro-apoptotic signals: increase of bcl-2 and decrease of bak/bax...
January 31, 2018: Diabetes
https://www.readbyqxmd.com/read/29382663/long-non-coding-rna-lncshgl-recruits-hnrnpa1-to-suppress-hepatic-gluconeogenesis-and-lipogenesis
#10
Junpei Wang, Weili Yang, Zhenzhen Chen, Ji Chen, Yuhong Meng, Biaoqi Feng, Libo Sun, Lin Dou, Jian Li, Qinghua Cui, Jichun Yang
Mammalian genomes encode a huge number of LncRNAs with unknown functions. This study determined the role and mechanism of a new LncRNA, LncRNA Suppressor of Hepatic Gluconeogenesis and Lipogenesis (LncSHGL), in regulating hepatic glucose/lipid metabolism. In the livers of obese mice and NAFLD patient, the expression levels of mouse LncSHGL and its human homologous LncRNA B4GALT1-AS1 were reduced. Hepatic LncSHGL restoration improved hyperglycemia, insulin resistance and steatosis in obese diabetic mice, whereas hepatic LncSHGL inhibition promoted fasting hyperglycemia and lipid deposition in normal mice...
January 30, 2018: Diabetes
https://www.readbyqxmd.com/read/29378767/perilipin-5-deletion-unmasks-an-endoplasmic-reticulum-stress-fibroblast-growth-factor-21-axis-in-skeletal-muscle
#11
Magdalene K Montgomery, Ruzaidi Mokhtar, Jacqueline Bayliss, Helena C Parkington, Victor M Suturin, Clinton R Bruce, Matthew J Watt
Lipid droplets are critical for the regulation of lipid metabolism, and dysregulated lipid metabolism contributes to the pathogenesis of several diseases including type 2 diabetes. We generated mice with muscle-specific deletion of the lipid droplet-associated protein, perilipin 5 (PLIN5, Plin5MKO ), and investigated PLIN5's role in regulating skeletal muscle lipid metabolism, intracellular signalling and whole-body metabolic homeostasis. High-fat feeding induced changes in muscle lipid metabolism of Plin5MKO mice, which included increased fatty acid oxidation and oxidative stress, but surprisingly, a reduction in inflammation and endoplasmic reticulum (ER) stress...
January 29, 2018: Diabetes
https://www.readbyqxmd.com/read/29362226/elovl4-mediated-production-of-very-long-chain-ceramides-stabilizes-tight-junctions-and-prevents-diabetes-induced-retinal-vascular-permeability
#12
Nermin M Kady, Xuwen Liu, Todd A Lydic, Meesum H Syed, Svetlana Navitskaya, Qi Wang, Sandra S Hammer, Sandra O'Reilly, Chao Huang, Sergey S Seregin, Andrea Amalfitano, Vince A Chiodo, Sanford L Boye, William W Hauswirth, David A Antonetti, Julia V Busik
Tight junctions (TJs) involve close apposition of transmembrane proteins between cells. While TJ proteins have been studied in detail, the role of lipids is largely unknown. We addressed the role of very long chain (VLC ≥26) ceramides in TJs using diabetes induced loss of blood-retinal barrier as a model. VLC fatty acids that incorporate into VLC ceramides are produced by elongase ELOVL4. ELOVL4 is significantly reduced in the diabetic retina. Overexpression of ELOVL4 significantly decreased basal permeability, inhibited VEGF and IL-1b induced permeability and prevented VEGF-induced decrease in occludin expression and border staining of TJ proteins; ZO-1 and claudin-5...
January 23, 2018: Diabetes
https://www.readbyqxmd.com/read/29343548/loss-of-b-cell-anergy-in-type-1-diabetes-is-associated-with-high-risk-hla-and-non-hla-disease-susceptibility-alleles
#13
Mia J Smith, Marynette Rihanek, Clive Wasserfall, Clayton E Mathews, Mark A Atkinson, Peter A Gottlieb, John C Cambier
Although B cells reactive with islet autoantigens are silenced by tolerance mechanisms in healthy individuals, they can become activated and contribute to development of type 1 diabetes. We previously demonstrated that high-affinity insulin-binding B cells (IBCs) occur exclusively in the anergic (BND) compartment in peripheral blood of healthy subjects. Consistent with their activation early in disease development, high-affinity IBCs are absent from the BND compartment of some first-degree relatives (FDRs) as well as all autoantibody positive pre-diabetic and new-onset type 1 diabetes patients, a time when they are found in pancreatic islets...
January 17, 2018: Diabetes
https://www.readbyqxmd.com/read/29343547/molecular-pathways-for-immune-recognition-of-preproinsulin-signal-peptide-in-type-1-diabetes
#14
Deborah Kronenberg-Versteeg, Martin Eichmann, Mark A Russell, Arnoud de Ru, Beate Hehn, Norkhairin Yusuf, Peter A van Veelen, Sarah J Richardson, Noel G Morgan, Marius K Lemberg, Mark Peakman
The signal peptide region of preproinsulin (PPI) contains epitopes targeted by human leucocyte antigen-A (HLA-A)-restricted (HLA-A0201, A2402) cytotoxic T-cells as part of the pathogenesis of β-cell destruction in type 1 diabetes. We extended PPI epitope discovery to disease-associated HLA-B*1801 and HLA-B*3906 (risk) and HLA-A*1101 and HLA-B*3801 (protective) alleles revealing that 4/6 alleles present epitopes derived from the signal peptide region. During co-translational translocation of PPI, its signal peptide is cleaved and retained within the endoplasmic reticulum (ER) membrane, implying it is processed for immune recognition outside of the canonical, proteasome-directed pathway...
January 17, 2018: Diabetes
https://www.readbyqxmd.com/read/29326366/highly-proliferative-alpha-cell-related-islet-endocrine-cells-in-human-pancreata
#15
Carol J Lam, Aaron R Cox, Daniel R Jacobson, Matthew M Rankin, Jake A Kushner
The proliferative response of non-β islet endocrine cells in response to type 1 diabetes (T1D) remains undefined. We quantified islet endocrine cell proliferation in a large collection of non-diabetic control and T1D human pancreata across a wide range of ages. Surprisingly, islet endocrine cells with abundant proliferation were present in many adolescent and young adult T1D pancreata. But, the proliferative islet endocrine cells were also present in similar abundance within control samples. We queried the proliferating islet cells with antisera against various islet hormones...
January 11, 2018: Diabetes
https://www.readbyqxmd.com/read/29326365/disruption-of-mitochondria-associated-endoplasmic-reticulum-membranes-mams-integrity-contributes-to-muscle-insulin-resistance-in-mice-and-humans
#16
Emily Tubbs, Stéphanie Chanon, Maud Robert, Nadia Bendridi, Gabriel Bidaux, Marie-Agnès Chauvin, Jingwei Ji-Cao, Christine Durand, Daphné Gauvrit-Ramette, Hubert Vidal, Etienne Lefai, Jennifer Rieusset
Modifications of the interactions between endoplasmic reticulum (ER) and mitochondria, defined as mitochondria-associated membranes (MAMs), were recently involved in the control of hepatic insulin action and glucose homeostasis, but with conflicting results. Whereas skeletal muscle is the primary site of insulin-mediated glucose uptake and the main target for alterations in insulin resistant states, the relevance of MAM integrity in muscle insulin resistance is unknown. Deciphering the importance of MAMs on muscle insulin signaling could help to clarify this controversy...
January 11, 2018: Diabetes
https://www.readbyqxmd.com/read/29321172/modest-decreases-in-endogenous-all-trans-retinoic-acid-produced-by-a-mouse-rdh10-heterozygote-provoke-major-abnormalities-in-adipogenesis-and-lipid-metabolism
#17
Di Yang, Marta G Vuckovic, Carolyn P Smullin, Myeongcheol Kim, Christabel Pui-See Lo, Emily Devericks, Hong Sik Yoo, Milena Tintcheva, Yinghua Deng, Joseph L Napoli
Pharmacological dosing of all-trans-retinoic acid (atRA) controls adiposity in rodents by inhibiting adipogenesis and inducing fatty acid oxidation. Retinol dehydrogenases (Rdh) catalyze the first reaction that activate retinol into atRA. This study examined post-natal contributions of Rdh10 to atRA biosynthesis and physiological functions of endogenous atRA. Embryonic fibroblasts from Rdh10 heterozygote hypomorphs or with a total Rdh10 knockout exhibit decreased atRA biosynthesis and escalated adipogenesis...
January 10, 2018: Diabetes
https://www.readbyqxmd.com/read/29321171/sgk1-foxo3-signaling-in-hypothalamic-pomc-neurons-mediates-glucocorticoid-increased-adiposity
#18
Yalan Deng, Yuzhong Xiao, Feixiang Yuan, Yaping Liu, Xiaoxue Jiang, Jiali Deng, Geza Fejes-Toth, Aniko Naray-Fejes-Toth, Shanghai Chen, Yan Chen, Hao Ying, Qiwei Zhai, Yousheng Shu, Feifan Guo
Although central nervous system has been implicated in glucocorticoid-induced fat mass gain, the underlying mechanisms are poorly understood. The aim of our current study was to investigate the possible involvement of hypothalamic serum- and glucocorticoid-regulated kinase 1 (SGK1) in glucocorticoid-increased adiposity. It is well-known that SGK1 expression is induced by acute glucocorticoid treatment, interestingly, we found its expression was decreased in the arcuate nucleus of the hypothalamus, including POMC neurons, following chronic dexamethasone (Dex) treatment...
January 10, 2018: Diabetes
https://www.readbyqxmd.com/read/29317436/the-diabetes-gene-and-wnt-pathway-effector-tcf7l2-regulates-adipocyte-development-and-function
#19
Xi Chen, Ayala Iriscilla, Chris Shannon, Marcel Fourcaudot, Nikhil K Acharya, Christopher P Jenkinson, Sami Heikkinen, Luke Norton
The gene encoding for transcription factor 7-like 2 (TCF7L2) is the strongest type 2 diabetes (T2DM) candidate gene discovered to date. The TCF7L2 protein is a key transcriptional effector of the Wnt/β-catenin signaling pathway, which is an important developmental pathway that negatively regulates adipogenesis. However, the precise role that TCF7L2 plays in the development and function of adipocytes remains largely unknown. Using a combination of in vitro approaches, we first show that TCF7L2 protein is increased during adipogenesis in 3T3-L1 cells and primary adipocyte stem cells (ASC), and that TCF7L2 expression is required for the regulation of Wnt signaling during adipogenesis...
January 9, 2018: Diabetes
https://www.readbyqxmd.com/read/29317435/skeletal-muscle-specific-deletion-of-mkp-1-reveals-a-p38-mapk-jnk-akt-signaling-node-that-regulates-obesity-induced-insulin-resistance
#20
Ahmed Lawan, Kisuk Min, Lei Zhang, Alberto Canfran-Duque, Michael J Jurczak, Joao Paulo G Camporez, Yaohui Nie, Timothy P Gavin, Gerald I Shulman, Carlos Hernandez-Fernando, Anton M Bennett
Stress responses promote obesity and insulin resistance, in part, by activating the stress-responsive mitogen-activated protein kinases (MAPKs), p38 MAPK and c-Jun NH2 kinase (JNK). Stress also induces expression of MAPK phosphatase-1 (MKP-1), which inactivates both JNK and p38 MAPK. However, the equilibrium between JNK/p38 MAPK and MKP-1 signaling in the development of obesity and insulin resistance is unclear. Skeletal muscle is a major tissue involved in energy expenditure and glucose metabolism. In skeletal muscle, MKP-1 is upregulated in high fat-diet fed mice and in skeletal muscle of obese humans...
January 9, 2018: Diabetes
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