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Glucose transporter deficiency

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https://www.readbyqxmd.com/read/29906877/chitosugar-translocation-by-an-unexpressed-monomeric-protein-channel
#1
H Sasimali M Soysa, Wipa Suginta, Watcharaporn Moonsap, M F Smith
The outer membrane protein channel EcChiP, associated with a silent gene in E. coli, is a monomeric chitoporin. In a glucose-deficient environment, E. coli can express the ChiP gene to exploit chitin degradation products. Single-channel small ion current measurements, which reveal the dynamics of single sugar molecules trapped in channel, are used here to study the exotic transport of chitosugars by E. coli. Molecules escape from the channel on multiple timescales. Voltage-dependent trapping rates observed for charged chitosan molecules, as well as model calculations, indicate that the rapid escape processes are those in which the molecule escapes back to the side of the membrane from which it originated...
May 2018: Physical Review. E
https://www.readbyqxmd.com/read/29903445/laboratory-investigations
#2
Eugen Boltshauser, Konrad P Weber
This chapter deals with chemical and hematologic investigations which are often considered in the diagnostic workup of subacute to chronic cerebellar ataxias. Relevant investigations in blood (serum, plasma), urine, and cerebrospinal fluid are discussed. Particular attention is paid to early diagnosis of treatable metabolic ataxias (such as abetalipoproteinemia, coenzyme Q10 deficiency, cerebrotendinous xanthomatosis, glucose transporter type 1 deficiency, Refsum disease, and vitamin E deficiency), but autoimmune ataxias, other vitamin deficiencies, and endocrine disorders should also be kept in mind...
2018: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/29899766/actual-insights-into-treatable-inborn-errors-of-metabolism-causing-epilepsy
#3
REVIEW
Mario Mastrangelo
This review offers an update on a group of inborn errors of metabolism causing severe epilepsy with the onset in pediatric age (but also other neurological manifestations such as developmental delay or movement disorders) with available effective or potentially effective treatments. The main pathogenic and clinical features and general recommendations for the diagnostic and therapeutic workup of the following disorders are discussed: vitamin B6 -dependent epilepsies, cerebral folate deficiency, congenital disorders of serine metabolism, biotinidase deficiency, inborn errors of creatine metabolism, molybdenum cofactor deficiency, and glucose transporter 1 deficiency...
January 2018: Journal of Pediatric Neurosciences
https://www.readbyqxmd.com/read/29899725/long-term-effect-of-gpi-dbs-in-a-patient-with-generalized-dystonia-due-to-glut1-deficiency-syndrome
#4
Idil Hanci, Christoph Kamm, Marlieke Scholten, Lorenzo P Roncoroni, Yvonne Weber, Rejko Krüger, Christian Plewnia, Alireza Gharabaghi, Daniel Weiss
Treatment outcomes from pallidal deep brain stimulation are highly heterogeneous reflecting the phenotypic and etiologic spectrum of dystonia. Treatment stratification to neurostimulation therapy primarily relies on the phenotypic motor presentation; however, etiology including genetic factors are increasingly recognized as modifiers of treatment outcomes. Here, we describe a 53 year-old female patient with a progressive generalized dystonia since age 25. The patient underwent deep brain stimulation of the globus pallidus internus (GPi-DBS) at age 44...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29875324/smooth-muscle-glucose-metabolism-promotes-monocyte-recruitment-and-atherosclerosis-in-a-mouse-model-of-metabolic-syndrome
#5
Valerie Z Wall, Shelley Barnhart, Jenny E Kanter, Farah Kramer, Masami Shimizu-Albergine, Neeta Adhikari, Thomas N Wight, Jennifer L Hall, Karin E Bornfeldt
Metabolic syndrome contributes to cardiovascular disease partly through systemic risk factors. However, local processes in the artery wall are becoming increasingly recognized to exacerbate atherosclerosis both in mice and humans. We show that arterial smooth muscle cell (SMC) glucose metabolism markedly synergizes with metabolic syndrome in accelerating atherosclerosis progression, using a low-density lipoprotein receptor-deficient mouse model. SMCs in proximity to atherosclerotic lesions express increased levels of the glucose transporter GLUT1...
June 7, 2018: JCI Insight
https://www.readbyqxmd.com/read/29873261/banxia-xiexin-decoction-ameliorated-cognition-via-the-regulation-of-insulin-pathways-and-glucose-transporters-in-the-hippocampus-of-appswe-ps1de9-mice
#6
Fang Chen, Yingkun He, Pengwen Wang, Peng Wei, Huili Feng, Yingxue Rao, Jing Shi, Jinzhou Tian
Reduced glucose utilization and deficient energy metabolism that occur in the early stages of Alzheimer's disease correlate with impaired cognition, and this information is evidence that Alzheimer's disease is a metabolic disease that is associated with brain insulin/insulin-like growth factor resistance. This research aimed to investigate the effects of Banxia Xiexin decoction (BXD) on cognitive deficits in APPswe/PS1dE9 double transgenic mice and verify the hypothesis that BXD treatment improves cognitive function via improving insulin signalling, glucose metabolism and synaptic plasticity in the hippocampus of APPswe/PS1dE9 double transgenic mice...
January 2018: International Journal of Immunopathology and Pharmacology
https://www.readbyqxmd.com/read/29860442/laboratory-evolution-of-a-glucose-phosphorylation-deficient-arabinose-fermenting-s-cerevisiae-strain-reveals-mutations-in-gal2-that-enable-glucose-insensitive-l-arabinose-uptake
#7
Maarten D Verhoeven, Jasmine M Bracher, Jeroen G Nijland, Jonna Bouwknegt, Jean-Marc G Daran, Arnold J M Driessen, Antonius J A van Maris, Jack T Pronk
Cas9-assisted genome editing was used to construct an engineered glucose-phosphorylation-negative S. cerevisiae strain, expressing the Lactobacillus plantaruml-arabinose pathway and the Penicillium chrysogenum transporter PcAraT. This strain, which showed a growth rate of 0.26 h-1 on l-arabinose in aerobic batch cultures, was subsequently evolved for anaerobic growth on l-arabinose in the presence of d-glucose and d-xylose. In four strains isolated from two independent evolution experiments the galactose-transporter gene GAL2 had been duplicated, with all alleles encoding Gal2N376T or Gal2N376I substitutions...
May 31, 2018: FEMS Yeast Research
https://www.readbyqxmd.com/read/29768946/neuroprotective-role-of-astroglia-in-parkinson-disease-by-reducing-oxidative-stress-through-dopamine-induced-activation-of-pentose-phosphate-pathway
#8
Kyoko Mashima, Shinichi Takahashi, Kazushi Minami, Yoshikane Izawa, Takato Abe, Naoki Tsukada, Takako Hishiki, Makoto Suematsu, Mayumi Kajimura, Norihiro Suzuki
Oxidative stress plays an important role in the onset and progression of Parkinson disease. Although released dopamine at the synaptic terminal is mostly reabsorbed by dopaminergic neurons, some dopamine is presumably taken up by astroglia. This study examined the dopamine-induced astroglial protective function through the activation of the pentose-phosphate pathway (PPP) to reduce reactive oxygen species (ROS). In vitro experiments were performed using striatal neurons and cortical or striatal astroglia prepared from Sprague-Dawley rats or C57BL/6 mice...
January 2018: ASN Neuro
https://www.readbyqxmd.com/read/29748289/regulation-of-insulin-receptor-pathway-and-glucose-metabolism-by-cd36-signaling
#9
Dmitri Samovski, Pallavi Dhule, Terri Pietka, Miriam Jacome-Sosa, Eric Penrose, Ni-Huiping Son, Robert C Flynn, Kooresh I Shoghi, Krzysztof L Hyrc, Ira J Goldberg, Eric R Gamazon, Nada A Abumrad
During reduced energy intake, skeletal muscle maintains homeostasis by rapidly suppressing insulin-stimulated glucose utilization. Loss of this adaptation is observed with deficiency of the fatty acid transporter CD36. A similar loss is also characteristic of the insulin resistant state where CD36 is dysfunctional. To elucidate what links CD36 to muscle glucose utilization we examined whether CD36 signaling might influence insulin action. First, we show that CD36 deletion specific to skeletal muscle reduces expression of insulin signaling and glucose metabolism genes...
May 10, 2018: Diabetes
https://www.readbyqxmd.com/read/29740774/sirtuin-signaling-controls-mitochondrial-function-in-glycogen-storage-disease-type-ia
#10
Jun-Ho Cho, Goo-Young Kim, Brian C Mansfield, Janice Y Chou
Glycogen storage disease type Ia (GSD-Ia) deficient in glucose-6-phosphatase-α (G6Pase-α) is a metabolic disorder characterized by impaired glucose homeostasis and a long-term complication of hepatocellular adenoma/carcinoma (HCA/HCC). Mitochondrial dysfunction has been implicated in GSD-Ia but the underlying mechanism and its contribution to HCA/HCC development remain unclear. We have shown that hepatic G6Pase-α deficiency leads to downregulation of sirtuin 1 (SIRT1) signaling that underlies defective hepatic autophagy in GSD-Ia...
May 8, 2018: Journal of Inherited Metabolic Disease
https://www.readbyqxmd.com/read/29740087/the-lactose-operon-from-lactobacillus-casei-is-involved-in-the-transport-and-metabolism-of-the-human-milk-oligosaccharide-core-2-n-acetyllactosamine
#11
Gonzalo N Bidart, Jesús Rodríguez-Díaz, Gaspar Pérez-Martínez, María J Yebra
The lactose operon (lacTEGF) from Lactobacillus casei strain BL23 has been previously studied. The lacT gene codes for a transcriptional antiterminator, lacE and lacF for the lactose-specific phosphoenolpyruvate: phosphotransferase system (PTSLac ) EIICB and EIIA domains, respectively, and lacG for the phospho-β-galactosidase. In this work, we have shown that L. casei is able to metabolize N-acetyllactosamine (LacNAc), a disaccharide present at human milk and intestinal mucosa. The mutant strains BL153 (lacE) and BL155 (lacF) were defective in LacNAc utilization, indicating that the EIICB and EIIA of the PTSLac are involved in the uptake of LacNAc in addition to lactose...
May 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29738435/crebh-regulates-systemic-glucose-and-lipid-metabolism
#12
REVIEW
Yoshimi Nakagawa, Hitoshi Shimano
The cyclic adenosine monophosphate (cAMP)-responsive element-binding protein H (CREBH, encoded by CREB3L3) is a membrane-bound transcriptional factor that primarily localizes in the liver and small intestine. CREBH governs triglyceride metabolism in the liver, which mediates the changes in gene expression governing fatty acid oxidation, ketogenesis, and apolipoproteins related to lipoprotein lipase (LPL) activation. CREBH in the small intestine reduces cholesterol transporter gene Npc1l1 and suppresses cholesterol absorption from diet...
May 8, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29738274/renal-injury-in-seipin-deficient-lipodystrophic-mice-and-its-reversal-by-adipose-tissue-transplantation-or-leptin-administration-alone-adipose-tissue-kidney-crosstalk
#13
Xue-Jing Liu, Xiao-Yue Wu, Huan Wang, Su-Xia Wang, Wei Kong, Ling Zhang, George Liu, Wei Huang
Seipin deficiency is responsible for type 2 congenital generalized lipodystrophy with severe loss of adipose tissue (AT) and could lead to renal failure in humans. However, the effect of Seipin on renal function is poorly understood. Here we report that Seipin knockout (SKO) mice exhibited impaired renal function, enlarged glomerular and mesangial surface areas, renal depositions of lipid, and advanced glycation end products. Elevated glycosuria and increased electrolyte excretion were also detected. Relative renal gene expression in fatty acid oxidation and reabsorption pathways were impaired in SKO mice...
May 8, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29731652/adjunctive-therapy-for-glucose-control-in-patients-with-type-1-diabetes
#14
REVIEW
Kira Harris, Cassie Boland, Lisa Meade, Dawn Battise
Type 1 diabetes mellitus (T1DM) is characterized by relative or absolute insulin deficiency. Despite treatment with insulin therapy, glycemic goals are not always met, and insulin therapy is sometimes limited by adverse effects, including hypoglycemia and weight gain. Several adjunctive therapies have been evaluated in combination with insulin in patients with T1DM to improve glycemic control while minimizing adverse effects. Pramlintide, an amylin analog, can improve glycemic control, primarily through lowering postprandial blood glucose levels...
2018: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
https://www.readbyqxmd.com/read/29723855/dioleoylphosphoethanolamine-retains-cell-surface-glut4-by-inhibiting-pkc%C3%AE-driven-internalization
#15
Tomoyuki Nishizaki
BACKGROUND/AIMS: Phosphatidylethanolamine, a component of the plasma membrane, regulates diverse cellular processes. The present study investigated the role of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine (DOPE) in the trafficking of the glucose transporter GLUT4 and the glucose homeostasis. METHODS: Monitoring of GLUT4 trafficking, GLUT4 internalization assay, and glucose uptake assay were carried out using differentiated 3T3-L1-GLUT4myc adipocytes. Akt1/2 and PKC isozymes were knocked-down by transfecting each siRNA...
April 26, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29721633/decreased-vmat2-in-the-pancreas-of-humans-with-type-2-diabetes-mellitus-measured-in-vivo-by-pet-imaging
#16
Gary W Cline, Mika Naganawa, Laigao Chen, Kristin Chidsey, Santos Carvajal-Gonzalez, Sylvester Pawlak, Michelle Rossulek, Yanwei Zhang, Jason Bini, Timothy J McCarthy, Richard E Carson, Roberto A Calle
AIMS/HYPOTHESIS: The progressive loss of beta cell function is part of the natural history of type 2 diabetes. Autopsy studies suggest that this is, in part, due to loss of beta cell mass (BCM), but this has not been confirmed in vivo. Non-invasive methods to quantify BCM may contribute to a better understanding of type 2 diabetes pathophysiology and the development of therapeutic strategies. In humans, the localisation of vesicular monoamine transporter type 2 (VMAT2) in beta cells and pancreatic polypeptide cells, with minimal expression in other exocrine or endocrine pancreatic cells, has led to its development as a measure of BCM...
May 2, 2018: Diabetologia
https://www.readbyqxmd.com/read/29719821/the-physiopathological-role-of-the-exchangers-belonging-to-the-slc37-family
#17
REVIEW
Anna Rita Cappello, Rosita Curcio, Rosamaria Lappano, Marcello Maggiolini, Vincenza Dolce
The human SLC37 gene family includes four proteins SLC37A1-4, localized in the endoplasmic reticulum (ER) membrane. They have been grouped into the SLC37 family due to their sequence homology to the bacterial organophosphate/phosphate (Pi) antiporter. SLC37A1-3 are the less characterized isoforms. SLC37A1 and SLC37A2 are Pi-linked glucose-6-phosphate (G6P) antiporters, catalyzing both homologous (Pi/Pi) and heterologous (G6P/Pi) exchanges, whereas SLC37A3 transport properties remain to be clarified. Furthermore, SLC37A1 is highly homologous to the bacterial glycerol 3-phosphate permeases, so it is supposed to transport also glycerol-3-phosphate...
2018: Frontiers in Chemistry
https://www.readbyqxmd.com/read/29719252/role-of-selenof-as-a-gatekeeper-of-secreted-disulfide-rich-glycoproteins
#18
Sun Hee Yim, Robert A Everley, Frank A Schildberg, Sang-Goo Lee, Andrea Orsi, Zachary R Barbati, Kutay Karatepe, Dmitry E Fomenko, Petra A Tsuji, Hongbo R Luo, Steven P Gygi, Roberto Sitia, Arlene H Sharpe, Dolph L Hatfield, Vadim N Gladyshev
Selenof (15-kDa selenoprotein; Sep15) is an endoplasmic reticulum (ER)-resident thioredoxin-like oxidoreductase that occurs in a complex with UDP-glucose:glycoprotein glucosyltransferase. We found that Selenof deficiency in mice leads to elevated levels of non-functional circulating plasma immunoglobulins and increased secretion of IgM during in vitro splenic B cell differentiation. However, Selenof knockout animals show neither enhanced bacterial killing capacity nor antigen-induced systemic IgM activity, suggesting that excess immunoglobulins are not functional...
May 1, 2018: Cell Reports
https://www.readbyqxmd.com/read/29719117/decreased-levels-of-keratin-8-sensitizes-mice-to-streptozotocin-induced-diabetes
#19
C M Alam, J S G Silvander, T O Helenius, D M Toivola
AIM: Diabetes is a result of an interplay between genetic, environmental and lifestyle factors. Keratin intermediate filaments are stress proteins in epithelial cells and keratin mutations predispose to several human diseases. However, the involvement of keratins in diabetes is not well known. K8 and its partner K18 are the main β-cell keratins, and knockout of K8 (K8-/- ) in mice causes mislocalization of glucose transporter 2, mitochondrial defects, reduced insulin content, and altered systemic glucose/insulin control...
May 2, 2018: Acta Physiologica
https://www.readbyqxmd.com/read/29697537/bariatric-surgery-and-gene-expression-in-the-gut
#20
Priscila Sala, M L Corrêa-Giannella, Dan L Waitzberg
PURPOSE OF REVIEW: The current review provides an overview of recent literature on new findings related to bariatric surgery and gut gene expression. RECENT FINDINGS: Bariatric surgery modulates the expression of intestinal genes. Experimental and clinical investigations have demonstrated the association of gut rearrangement with changes in intestinal expression of genes related to glucose metabolism. Recent data suggest that bariatric surgery also affects expression of genes belonging to other pathways, including nutrient transporters and metabolism of vitamin B12, decreasing pathway-encoding genes that may contribute to vitamin B12 deficiency in the postoperative period...
July 2018: Current Opinion in Clinical Nutrition and Metabolic Care
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