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Glucose transporter deficiency

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https://www.readbyqxmd.com/read/29216217/the-emerging-role-of-asc-in-dendritic-cell-metabolism-during-chlamydia-infection
#1
Danielle N McKeithen, Yusuf O Omosun, Khamia Ryans, Jing Mu, Zhonglin Xie, Tankya Simoneaux, Uriel Blas-Machado, Francis O Eko, Carolyn M Black, Joseph U Igietseme, Qing He
Chlamydia trachomatis is a bacterial agent that causes sexually transmitted infections worldwide. The regulatory functions of dendritic cells (DCs) play a major role in protective immunity against Chlamydia infections. Here, we investigated the role of ASC in DCs metabolism and the regulation of DCs activation and function during Chlamydia infection. Following Chlamydia stimulation, maturation and antigen presenting functions were impaired in ASC-/- DCs compared to wild type (WT) DCs, in addition, ASC deficiency induced a tolerant phenotype in Chlamydia stimulated DCs...
2017: PloS One
https://www.readbyqxmd.com/read/29205673/mechanisms-of-ampk-in-the-maintenance-of-atp-balance-during-energy-metabolism
#2
REVIEW
Rong Ke, Qicao Xu, Cong Li, Lingyu Luo, Deqiang Huang
AMP-activated protein kinase (AMPK) is a conserved sensor of cellular energy change and is activated by increased AMP/ATP and/or ADP/ATP ratios. AMPK maintains the energy balance by decreasing the ATP-consuming processes such as transcription of synthetic fat genes and rRNA, the translation of ribosomal proteins, synthesis of cholesterol and fatty acid, while the metabolic pathways such as glucose and fatty transport, fatty acid oxidation, autophagy, mitochondrial synthesis and oxidative metabolism are increased to preserve ATP during energy deficiency...
December 4, 2017: Cell Biology International
https://www.readbyqxmd.com/read/29199027/10-patients-10-years-long-term-follow-up-of-cardiovascular-risk-factors-in-glut1-deficiency-treated-with-ketogenic-diet-therapies-a%C3%A2-prospective-multicenter-case-series
#3
Nicole Heussinger, Adela Della Marina, Andreas Beyerlein, Baerbel Leiendecker, Sofia Hermann-Alves, Robert Dalla Pozza, Joerg Klepper
BACKGROUND AND AIMS: Glut1 Deficiency (Glut1D) is caused by impaired glucose transport into brain. The resulting epileptic encephalopathy and movement disorders can be treated effectively by high-fat carbohydrate-restricted ketogenic diet therapies (KDT) mimicking fasting and providing ketones as an alternative cerebral fuel. Recently 6-24 months follow-ups of epileptic patients reported elevated blood lipids and intima thickening of the carotid artery raising concerns about potential cardiovascular risks by KDT...
November 11, 2017: Clinical Nutrition: Official Journal of the European Society of Parenteral and Enteral Nutrition
https://www.readbyqxmd.com/read/29144225/prevalence-of-genetic-disorders-and-glut1-deficiency-in-a-ketogenic-diet-clinic
#4
Stacy Hewson, Ledia Brunga, Matilde Fernandez Ojeda, Elizabeth Imhof, Jaina Patel, Maria Zak, Elizabeth J Donner, Jeff Kobayashi, Gajja S Salomons, Saadet Mercimek-Andrews
Between July of 2012 and December of 2014, 39 patients were enrolled prospectively to investigate the prevalence of glucose transporter 1 (GLUT1) deficiency in a ketogenic diet clinic. None of them had GLUT1 deficiency. All patients seen in the same clinic within the same period were reviewed retrospectively. A total of 18 of these 85 patients had a genetic diagnosis, including GLUT1 deficiency, pathogenic copy number variants, congenital disorder of glycosylation, neuronal ceroid lipofuscinosis type II, mitochondrial disorders, tuberous sclerosis, lissencephaly, and SCN1A-, SCN8A-, and STXBP1-associated epileptic encephalopathies...
November 16, 2017: Canadian Journal of Neurological Sciences. le Journal Canadien des Sciences Neurologiques
https://www.readbyqxmd.com/read/29134558/development-of-hyperkalemia-following-treatment-with-dapagliflozin-dapa-in-a-patient-with-type-2-diabetes-after-bilateral-adrenalectomy
#5
Daichi Miyaoka, Akihiro Tsuda, Noriyuki Hayashi, Norikazu Toi, Akiyo Yamasaki, Yuki Nagata, Shinya Nakatani, Masafumi Kurajoh, Shinsuke Yamada, Tomoaki Morioka, Yasuo Imanishi, Masanori Emoto, Masaaki Inaba
Dapagliflozin (DAPA), a sodium-glucose co-transporter 2 (SGLT2) inhibitor, is known to have a beneficial diuretic effect, in addition to a glucose-lowering effect. Although SGLT2 inhibitor has been reported, the increase of hyperkalemia in patients treated with renin-angiotensin-aldosterone system (RAAS) inhibitors, their mechanism of action is unclear. We report the first case of a type 2 diabetes (T2DM) patient with potential mineralocorticoid deficiency who developed hyperkalemia after administration of DAPA...
November 13, 2017: CEN Case Reports
https://www.readbyqxmd.com/read/29133412/cell-autonomous-adiposity-through-increased-cell-surface-glut4-due-to-ankyrin-b-deficiency
#6
Damaris N Lorenzo, Vann Bennett
Obesity typically is linked to caloric imbalance as a result of overnutrition. Here we propose a cell-autonomous mechanism for adiposity as a result of persistent cell surface glucose transporter type 4 (GLUT4) in adipocytes resulting from impaired function of ankyrin-B (AnkB) in coupling GLUT4 to clathrin-mediated endocytosis. Adipose tissue-specific AnkB-KO mice develop obesity and progressive pancreatic islet dysfunction with age or high-fat diet (HFD). AnkB-deficient adipocytes exhibit increased lipid accumulation associated with increased glucose uptake and impaired endocytosis of GLUT4...
November 13, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29111970/complementation-of-a-metk-deficient-e-coli-strain-with-heterologous-adomet-synthetase-genes
#7
Gwenn G Parungao, Mojun Zhao, Qinzhe Wang, Stephen P Zano, Ronald E Viola, Robert M Blumenthal
S-adenosyl-l-methionine (AdoMet) is an essential metabolite, playing a wide variety of metabolic roles. The enzyme that produces AdoMet from l-methionine and ATP (methionine adenosyltransferase, MAT) is thus an attractive target for anti-cancer and antimicrobial agents. It would be very useful to have a system that allows rapid identification of species-specific inhibitors of this essential enzyme. A previously generated E. coli strain, lacking MAT (∆metK) but containing a heterologous AdoMet transporter, was successfully complemented with heterologous metK genes from several bacterial pathogens, as well as with MAT genes from a fungal pathogen and Homo sapiens...
November 7, 2017: Microbiology
https://www.readbyqxmd.com/read/29091932/essential-roles-of-aspartate-aminotransferase-1-and-vesicular-glutamate-transporters-in-%C3%AE-cell-glutamate-signaling-for-incretin-induced-insulin-secretion
#8
Naoya Murao, Norihide Yokoi, Kohei Honda, Guirong Han, Tomohide Hayami, Ghupurjan Gheni, Harumi Takahashi, Kohtaro Minami, Susumu Seino
Incretins (GLP-1 and GIP) potentiate insulin secretion through cAMP signaling in pancreatic β-cells in a glucose-dependent manner. We recently proposed a mechanistic model of incretin-induced insulin secretion (IIIS) that requires two critical processes: 1) generation of cytosolic glutamate through the malate-aspartate (MA) shuttle in glucose metabolism and 2) glutamate transport into insulin granules by cAMP signaling to promote insulin granule exocytosis. To directly prove the model, we have established and characterized CRISPR/Cas9-engineered clonal mouse β-cell lines deficient for the genes critical in these two processes: aspartate aminotransferase 1 (AST1, gene symbol Got1), a key enzyme in the MA shuttle, which generates cytosolic glutamate, and the vesicular glutamate transporters (VGLUT1, VGLUT2, and VGLUT3, gene symbol Slc17a7, Slc17a6, and Slc17a8, respectively), which participate in glutamate transport into secretory vesicles...
2017: PloS One
https://www.readbyqxmd.com/read/29077094/non-oncogenic-roles-of-tap73-from-multiciliogenesis-to-metabolism
#9
REVIEW
Alice Nemajerova, Ivano Amelio, Jakob Gebel, Volker Dötsch, Gerry Melino, Ute M Moll
The p53 family of transcription factors (p53, p63 and p73) covers a wide range of functions critical for development, homeostasis and health of mammals across their lifespan. Beside the well-established tumor suppressor role, recent evidence has highlighted novel non-oncogenic functions exerted by p73. In particular, p73 is required for multiciliated cell (MCC) differentiation; MCCs have critical roles in brain and airways to move fluids across epithelial surfaces and to transport germ cells in the reproductive tract...
October 27, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29073628/transient-congenital-hypothyroidism-alters-gene-expression-of-glucose-transporters-and-impairs-glucose-sensing-apparatus-in-young-and-aged-offspring-rats
#10
Hanieh Gholami, Sajad Jeddi, Azita Zadeh-Vakili, Khadije Farrokhfall, Fatemeh Rouhollah, Maryam Zarkesh, Mahboubeh Ghanbari, Asghar Ghasemi
BACKGROUND/AIMS: Transient congenital hypothyroidism (TCH) could disturb carbohydrate metabolism in adulthood. Aging is associated with increased risk of type 2 diabetes. This study aims to address effects of TCH on mRNA expressions of glucose transporters (GLUTs) and glucokinase (GcK) in islets and insulin target tissues of aged offspring rats. METHODS: The TCH group received water containing 0.025% 6-propyl-2-thiouracil during gestation. Offspring from control and TCH groups (n=6 in each group) were followed until month 19...
October 27, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29066623/reconciling-contradictory-findings-glucose-transporter-1-glut1-functions-as-an-oligomer-of-allosteric-alternating-access-transporters
#11
Kenneth P Lloyd, Ogooluwa A Ojelabi, Julie K De Zutter, Anthony Carruthers
Recent structural studies suggest that glucose transporter 1 (GLUT1)-mediated sugar transport is mediated by an alternating access transporter that successively presents exofacial (e2) and endofacial (e1) substrate-binding sites. Transport studies, however, indicate multiple, interacting (allosteric), and co-existent, exo- and endofacial GLUT1 ligand-binding sites. The present study asks whether these contradictory conclusions result from systematic analytical error or reveal a more fundamental relationship between transporter structure and function...
October 24, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29066466/dgk%C3%AE-deficiency-protects-against-peripheral-insulin-resistance-and-improves-energy-metabolism
#12
Boubacar Benziane, Melissa L Borg, Robby Z Tom, Isabelle Riedl, Julie Massart, Marie Björnholm, Marc Gilbert, Alexander V Chibalin, Juleen R Zierath
Diacylglycerol kinases (DGK) regulate the balance between diacylglycerol (DAG) and phosphatidic acid. DGKζ is highly abundant in skeletal muscle and induces fiber hypertrophy. We hypothesized DGKζ influences functional and metabolic adaptions in skeletal muscle and whole body fuel utilization. DAG content was increased in skeletal muscle and adipose tissue, but unaltered in liver of DGKζ knockout (KO) mice. Linear growth, body weight, fat mass, and lean mass was reduced in DGKζ KO versus wild-type mice...
October 24, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/29029025/insulin-deficient-mouse-%C3%AE-cells-do-not-fully-mature-but-can-be-remedied-through-insulin-replacement-by-islet-transplantation
#13
Adam Ramzy, Majid Mojibian, Timothy J Kieffer
Insulin receptor insufficiency in β-cells leads to impaired insulin secretion and reduced β-cell hyperplasia in response to hyperglycemia. Selective insulin receptor deficiency in β-cells in later embryological development may lead to compensatory β-cell hyperplasia. Though these findings suggest insulin signaling on the β-cell is important for β-cell function, they are confounded by loss of signaling by the IGFs through the insulin receptor. To determine if insulin itself is necessary for β-cell development and maturation, we performed a characterization of pancreatic islets in mice with deletions of both non-allelic insulin genes (Ins1-/-Ins2-/-)...
September 27, 2017: Endocrinology
https://www.readbyqxmd.com/read/29018245/transient-postnatal-overfeeding-causes-liver-stress-induced-premature-senescence-in-adult-mice
#14
Catherine Yzydorczyk, Na Li, Hassib Chehade, Dolores Mosig, Mickael Bidho, Basile Keshavjee, Jean Baptiste Armengaud, Katya Nardou, Benazir Siddeek, Mohamed Benahmed, Catherine Vergely, Umberto Simeoni
Unbalanced nutrition early in life is increasingly recognized as an important factor in the development of chronic, non-communicable diseases at adulthood, including metabolic diseases. We aimed to determine whether transient postnatal overfeeding (OF) leads to liver stress-induced premature senescence (SIPS) of hepatocytes in association with liver structure and hepatic function alterations. Litters sizes of male C57BL/6 mice were adjusted to 9 pups (normal feeding, NF) or reduced to 3 pups during the lactation period to induce transient postnatal OF...
October 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28993322/comparative-study-of-expression-and-activity-of-glucose-transporters-between-stem-cell-derived-brain-microvascular-endothelial-cells-and-hcmec-d3-cells
#15
COMPARATIVE STUDY
Abraham J Al-Ahmad
Glucose constitutes a major source of energy of mammalian brains. Glucose uptake at the blood-brain barrier (BBB) occurs through a facilitated glucose transport, through glucose transporter 1 (GLUT1), although other isoforms have been described at the BBB. Mutations in GLUT1 are associated with the GLUT1 deficiency syndrome, yet none of the current in vitro models of the human BBB maybe suited for modeling such a disorder. In this study, we investigated the expression of glucose transporters and glucose diffusion across brain microvascular endothelial cells (BMECs) derived from healthy patient-derived induced pluripotent stem cells (iPSCs)...
October 1, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28978056/vitamin-d-deficiency-causes-insulin-resistance-by-provoking-oxidative-stress-in-hepatocytes
#16
Sha Tao, Qi Yuan, Li Mao, Feng-Li Chen, Feng Ji, Zhao-Hui Cui
Vitamin D deficiency could cause insulin resistance. However, the underlying mechanisms are unclear. The 1α-Hydroxylase ["1α(OH)ase"] is a key enzyme for activate vitamin D3 synthesis. Here, we show that 1α(OH)ase stable knockdown by targeted shRNA led to vitamin D3 depletion in L02 hepatocytes. 1α(OH)ase silence also inhibited insulin-induced downstream signaling (IRS-1, ERK and AKT) transduction and glucose transporter 4 expression. Further, 1α(OH)ase shRNA in L02 hepatocytes led to significant reactive oxygen species production, p53-p21 activation and DNA damages...
September 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28976221/dapagliflozin-attenuates-human-vascular-endothelial-cell-activation-and-induces-vasorelaxation-a-potential-mechanism-for-inhibition-of-atherogenesis
#17
Tracey Gaspari, Iressa Spizzo, HongBin Liu, Yunshan Hu, Richard W Simpson, Robert E Widdop, Anthony E Dear
BACKGROUND: Sodium glucose transporter type 2 inhibitors may reduce cardiovascular events in type 2 diabetes. Our study aimed to determine the effect of the sodium glucose transporter type 2 inhibitor dapagliflozin on endothelial cell activation, vasoreactivity and atherogenesis using in vitro and in vivo models and identify associated molecular mechanisms. METHODS: In vitro studies utilised human vascular endothelial cells stimulated with tumour necrosis factor α or hyperglycaemic conditions...
October 1, 2017: Diabetes & Vascular Disease Research
https://www.readbyqxmd.com/read/28974775/biochemical-and-cellular-properties-of-insulin-receptor-signalling
#18
REVIEW
Rebecca A Haeusler, Timothy E McGraw, Domenico Accili
The mechanism of insulin action is a central theme in biology and medicine. In addition to the rather rare condition of insulin deficiency caused by autoimmune destruction of pancreatic β-cells, genetic and acquired abnormalities of insulin action underlie the far more common conditions of type 2 diabetes, obesity and insulin resistance. The latter predisposes to diseases ranging from hypertension to Alzheimer disease and cancer. Hence, understanding the biochemical and cellular properties of insulin receptor signalling is arguably a priority in biomedical research...
October 4, 2017: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/28974690/loss-of-endometrial-sodium-glucose-cotransporter-sglt1-is-detrimental-to-embryo-survival-and-fetal-growth-in-pregnancy
#19
Madhuri S Salker, Yogesh Singh, Ni Zeng, Hong Chen, Shaqiu Zhang, Anja T Umbach, Hajar Fakhri, Ursula Kohlhofer, Leticia Quintanilla-Martinez, Ruban R Peter Durairaj, Flavio S V Barros, Pavle Vrljicak, Sascha Ott, Sara Y Brucker, Diethelm Wallwiener, Ivana Vrhovac Madunić, Davorka Breljak, Ivan Sabolić, Hermann Koepsell, Jan J Brosens, Florian Lang
Embryo implantation requires a hospitable uterine environment. A key metabolic change that occurs during the peri-implantation period, and throughout early pregnancy, is the rise in endometrial glycogen content. Glycogen accumulation requires prior cellular uptake of glucose. Here we show that both human and murine endometrial epithelial cells express the high affinity Na(+)-coupled glucose carrier SGLT1. Ussing chamber experiments revealed electrogenic glucose transport across the endometrium in wild type (Slc5a1 (+/+)) but not in SGLT1 deficient (Slc5a1 (-/-)) mice...
October 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28973635/liver-directed-gene-therapy-for-murine-glycogen-storage-disease-type-ib
#20
Joon Hyun Kwon, Young Mok Lee, Jun-Ho Cho, Goo-Young Kim, Javier Anduaga, Matthew F Starost, Brian C Mansfield, Janice Y Chou
Glycogen storage disease type-Ib (GSD-Ib), deficient in the glucose-6-phosphate transporter (G6PT), is characterized by impaired glucose homeostasis, myeloid dysfunction, and long-term risk of hepatocellular adenoma (HCA). We examined the efficacy of G6PT gene therapy in G6pt-/- mice using recombinant adeno-associated virus (rAAV) vectors, directed by either the G6PC or the G6PT promoter/enhancer. Both vectors corrected hepatic G6PT deficiency in murine GSD-Ib but the G6PC promoter/enhancer was more efficacious...
November 15, 2017: Human Molecular Genetics
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