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Glucose transporter deficiency

Hikari Takeshita, Masao Takeda, Koichi Yamamoto, Hiromi Rakugi
OBJECTIVE: Angiotensin converting enzyme2 (ACE2), an enzyme that produces the Angiotensin 1-7(A1-7) from Angiotensin II, is considered to suppress organ damage by inhibition of the activation of renin-angiotensin system. We recently found that ACE2 deficiency in mice ameliorated insulin sensitivity of skeletal muscle with reduced expression of glucose transporter 4 and myocyte enhancer factor 2, an important transcription factor to maintain homeostasis of skeletal muscle. In this study, we investigated whether ACE2-A1-7 axis plays a protective role in aging-associated loss of skeletal muscle function in mice...
September 2016: Journal of Hypertension
Wen-Lian Chen, Yue-Ying Wang, Aihua Zhao, Li Xia, Guoxiang Xie, Mingming Su, Linjing Zhao, Jiajian Liu, Chun Qu, Runmin Wei, Cynthia Rajani, Yan Ni, Zhen Cheng, Zhu Chen, Sai-Juan Chen, Wei Jia
Rapidly proliferating leukemic progenitor cells consume substantial glucose, which may lead to glucose insufficiency in bone marrow. We show that acute myeloid leukemia (AML) cells are prone to fructose utilization with an upregulated fructose transporter GLUT5, which compensates for glucose deficiency. Notably, AML patients with upregulated transcription of the GLUT5-encoding gene SLC2A5 or increased fructose utilization have poor outcomes. Pharmacological blockage of fructose uptake ameliorates leukemic phenotypes and potentiates the cytotoxicity of the antileukemic agent, Ara-C...
September 28, 2016: Cancer Cell
Marina Diomedi, Ziv Gan-Or, Fabio Placidi, Patrick A Dion, Anna Szuto, Mario Bengala, Guy A Rouleau, Gian Luigi Gigli
Glucose transporter 1 (GLUT1) deficiency syndrome (GLUT1DS) was initially described in the early 90s as a sporadic clinical condition, characterized by seizures, motor and intellectual impairment with variable clinical presentation, and without a known genetic cause. Although causative mutations in SLC2A1 were later identified and much more is known about the disease, it still remains largely underdiagnosed. In the current study, a previously described Italian family was re-analyzed using whole exome sequencing and clinically re-evaluated...
October 7, 2016: European Journal of Medical Genetics
Tolunay Beker Aydemir, Catalina Troche, Min-Hyun Kim, Robert J Cousins
Zinc influences signaling pathways through controlled targeted zinc transport. Zinc transporter Zip14 KO mice display a phenotype which includes impaired intestinal barrier function with low-grade chronic inflammation, hyperinsulinemia and increased body fat which are signatures of diet-induced diabetes (type 2 diabetes) and obesity in humans. Hyperglycemia in type 2 diabetes and obesity is caused by insulin resistance. Insulin resistance results in inhibition of glucose uptake by liver and other peripheral tissues, principally adipose and muscle and with concurrently higher hepatic glucose production...
October 4, 2016: Journal of Biological Chemistry
Mareike Kavka, Andrea Polle
BACKGROUND: Phosphorus (P) is a major plant nutrient. It is transported into and allocated inside plants by four families of phosphate transporters (PHT1 to PHT4) with high or low affinity to phosphate. Here, we studied whole-plant P uptake kinetics and expression profiles of members of the PHT families under high, intermediate and low P availability in the woody crop poplar (Populus × canescens) in relation to plant performance. RESULTS: Poplars exhibited strong growth reduction and increased P use efficiency in response to lower P availabilities...
2016: BMC Plant Biology
Hikari Takeshita, Masao Takeda, Koichi Yamamoto, Hiromi Rakugi
OBJECTIVE: Angiotensin converting enzyme2 (ACE2), an enzyme that produces the Angiotensin 1-7(A1-7) from Angiotensin II, is considered to suppress organ damage by inhibition of the activation of renin-angiotensin system. We recently found that ACE2 deficiency in mice ameliorated insulin sensitivity of skeletal muscle with reduced expression of glucose transporter 4 and myocyte enhancer factor 2, an important transcription factor to maintain homeostasis of skeletal muscle. In this study, we investigated whether ACE2-A1-7 axis plays a protective role in aging-associated loss of skeletal muscle function in mice...
September 2016: Journal of Hypertension
Hu Zeng, Sivan Cohen, Cliff Guy, Sharad Shrestha, Geoffrey Neale, Scott A Brown, Caryn Cloer, Rigel J Kishton, Xia Gao, Ben Youngblood, Mytrang Do, Ming O Li, Jason W Locasale, Jeffrey C Rathmell, Hongbo Chi
Follicular helper T (Tfh) cells are crucial for germinal center (GC) formation and humoral adaptive immunity. Mechanisms underlying Tfh cell differentiation in peripheral and mucosal lymphoid organs are incompletely understood. We report here that mTOR kinase complexes 1 and 2 (mTORC1 and mTORC2) are essential for Tfh cell differentiation and GC reaction under steady state and after antigen immunization and viral infection. Loss of mTORC1 and mTORC2 in T cells exerted distinct effects on Tfh cell signature gene expression, whereas increased mTOR activity promoted Tfh responses...
September 20, 2016: Immunity
Laurent Bultot, Thomas E Jensen, Yu-Chiang Lai, Agnete L B Madsen, Caterina Collodet, Samanta Kviklyte, Maria Deak, Arash Yavari, Marc Foretz, Sahar Ghaffari, Mohamed Bellahcene, Houman Ashrafian, Mark H Rider, Erik A Richter, Kei Sakamoto
AMP-activated protein kinase (AMPK) plays diverse roles and coordinates complex metabolic pathways for maintenance of energy homeostasis. This could be explained by the fact that AMPK exists as multiple heterotrimer complexes comprising a catalytic α-subunit (α1 and α2) and regulatory β (β1 and β2)- and γ (γ1, γ2, γ3)-subunits, which are uniquely distributed across different cell types. There has been keen interest in developing specific and isoform-selective AMPK-activating drugs for therapeutic use and also as research tools...
October 1, 2016: American Journal of Physiology. Endocrinology and Metabolism
Anne Forand, Eugénie Koumakis, Alice Rousseau, Yohann Sassier, Clément Journe, Jean-François Merlin, Christine Leroy, Valérie Boitez, Patrice Codogno, Gérard Friedlander, Isabelle Cohen
The liver plays a central role in whole-body lipid and glucose homeostasis. Increasing dietary fat intake results in increased hepatic fat deposition, which is associated with a risk for development of insulin resistance and type 2 diabetes. In this study, we demonstrate a role for the phosphate inorganic transporter 1 (PiT1/SLC20A1) in regulating metabolism. Specific knockout of Pit1 in hepatocytes significantly improved glucose tolerance and insulin sensitivity, enhanced insulin signaling, and decreased hepatic lipogenesis...
September 6, 2016: Cell Reports
Nicole Ziegler, Khader Awwad, Beate Fisslthaler, Marco Reis, Kavi Devraj, Monica Corada, Simone Paolo Minardi, Elisabetta Dejana, Karl H Plate, Ingrid Fleming, Stefan Liebner
UNLABELLED: The canonical Wnt/β-catenin signaling pathway is crucial for blood-brain barrier (BBB) formation in brain endothelial cells. Although glucose transporter 1, claudin-3, and plasmalemma vesicular-associated protein have been identified as Wnt/β-catenin targets in brain endothelial cells, further downstream targets relevant to BBB formation and function are incompletely explored. By Affymetrix expression analysis, we show that the cytochrome P450 enzyme Cyp1b1 was significantly decreased in β-catenin-deficient mouse endothelial cells, whereas its close homolog Cyp1a1 was upregulated in an aryl hydrocarbon receptor-dependent manner, hence indicating that β-catenin is indispensable for Cyp1b1 but not for Cyp1a1 expression...
August 24, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Bingxian Xie, Qiaoli Chen, Liang Chen, Yang Sheng, Hong Yu Wang, Shuai Chen
The AS160 is a Rab-GTPase activating protein (RabGAP) with several other functional domains, and its deficiency in mice or human patients lowers glucose transporter-4 (GLUT4) protein levels and causes severe insulin resistance. How its deficiency causes diminished GLUT4 proteins remains unknown. We found that deletion of AS160 decreased GLUT4 levels in a cell/tissue autonomous manner. Consequently, skeletal muscle-specific deletion of AS160 caused postprandial hyperglycemia and hyperinsulinemia. The pathogenic effects of AS160 deletion are mainly, if not exclusively, due to the loss of its RabGAP function since the RabGAP inactive AS160(R917K) mutant mice phenocopied the AS160 knockout mice...
August 23, 2016: Diabetes
Shinya Hirayama, Yuichiro Hori, Zsolt Benedek, Tadashi Suzuki, Kazuya Kikuchi
Glucose transporter 4 (GLUT4) is an N-glycosylated protein that maintains glucose homeostasis by regulating the protein translocation. To date, it has been unclear whether the N-glycan of GLUT4 contributes to its intracellular trafficking. Here, to clarify the role of the N-glycan, we developed fluorogenic probes that label cytoplasmic and plasma-membrane proteins for multicolor imaging of GLUT4 translocation. One of the probes, which is cell impermeant, selectively detected exocytosed GLUT4. Using this probe, we verified the 'log' of the trafficking, in which N-glycan-deficient GLUT4 was transiently translocated to the cell membrane upon insulin stimulation and was rapidly internalized without retention on the cell membrane...
October 2016: Nature Chemical Biology
Luciane M Tomaz, Marina R Barbosa, Zahra Farahnak, Cristiani G Lagoeiro, Natalia S S Magosso, Jean-Marc Lavoie, Sérgio E A Perez
PURPOSE: This study investigated the effects of ovariectomy (Ovx) and 12 weeks of resistance training (RT) on gene expression of GLUT2, the main glucose transporter in the liver, and on PPARγ, a transcription factor known to target GLUT2 expression. METHODS: Forty Holtzman rats were divided into 5 groups: Sham-sedentary (Sed), Sham- RT, Ovx-Sed, Ovx-RT, and Ovx-Sed with hormone replacement (E2). The RT protocol consisted of sessions held every 72 h for 12 weeks, during which the animals performed 4 to 9 vertical climbs (1...
June 2016: Journal of Exercise Nutrition & Biochemistry
Yehui Du, Hao Chen, Zefeng Xuan, Wenfeng Song, Liangjie Hong, Danjing Guo, Hongchun Li, Biguang Tuo, Shusen Zheng, Penghong Song
BACKGROUND: Biliary tract obstruction is a common clinical problem. In this study, we attempted to understand the change in intestinal glucose absorption after biliary tract obstruction. METHODS: Experimental models of murine biliary duct ligation and external biliary drainage were established. Murine intestinal mucosal glucose absorption was examined with Ussing chambers according to the increase in the short-circuit current in vitro and blood glucose measurement after oral glucose in vivo...
August 2, 2016: Surgery
N Farhat, A Smaoui, M Laurence, B Porcheron, R Lemoine, C Abdelly, M Rabhi
Being the principal product of photosynthesis, sucrose is involved in many metabolic processes in plants. As magnesium (Mg) is phloem mobile, an inverse relationship between Mg shortage and sugar accumulation in leaves is often observed. Mg deficiency effects on carbohydrate contents and invertase activities were determined in Sulla carnosa Desf. Plants were grown hydroponically at different Mg concentrations (0.00, 0.01, 0.05 and 1.50 mM Mg) for one month. Mineral analysis showed that Mg contents were drastically diminished in shoots and roots mainly at 0...
August 4, 2016: Plant Biology
Imad Mohammad Dweikat, Issa Shaher Alawneh, Sami Fares Bahar, Mutaz Idrees Sultan
BACKGROUND: Fanconi-Bickel syndrome (FBS, OMIM 227810) is a rare autosomal recessive disease caused by a deficiency of glucose transporter 2 (GLUT2), a member of the facilitative glucose transporter family (Santer et al. J Inherit Metab Dis 21:191-194, 1998). The typical clinical picture is characterized by hepatorenal glycogen accumulation resulting in hepato- and nephromegaly, impaired utilization of glucose and galactose, proximal renal tubular dysfunction, rickets and severe short stature...
2016: BMC Research Notes
Ayako Fukunaka, Yoshio Fujitani
Pancreatic β cells contain the highest amount of zinc among cells within the human body, and hence, the relationship between zinc and diabetes has been a topic of great interest. While many studies demonstrating possible involvement of zinc deficiency in diabetes have been reported, precise mechanisms how zinc regulates glucose metabolism are still far from understood. Recent studies revealed that zinc can transmit signals that are driven by a variety of zinc transporters in a tissue and cell-type specific manner and deficiency in some zinc transporters may cause human diseases...
July 2016: Nihon Rinsho. Japanese Journal of Clinical Medicine
Chiara Ciccarese, Matteo Brunelli, Rodolfo Montironi, Michelangelo Fiorentino, Roberto Iacovelli, Daniel Heng, Giampaolo Tortora, Francesco Massari
The therapeutic landscape of renal cell carcinoma (RCC) has greatly expanded in the last decade. From being a malignancy orphan of effective therapies, kidney cancer has become today a tumor with several treatment options. Renal cell carcinoma (RCC) is a metabolic disease, being characterized by the dysregulation of metabolic pathways involved in oxygen sensing (VHL/HIF pathway alterations and the subsequent up-regulation of HIF-responsive genes such as VEGF, PDGF, EGF, and glucose transporters GLUT1 and GLUT4, which justify the RCC reliance on aerobic glycolysis), energy sensing (fumarate hydratase-deficient, succinate dehydrogenase-deficient RCC, mutations of HGF/MET pathway resulting in the metabolic Warburg shift marked by RCC increased dependence on aerobic glycolysis and the pentose phosphate shunt, augmented lipogenesis, and reduced AMPK and Krebs cycle activity) and/or nutrient sensing cascade (deregulation of AMPK-TSC1/2-mTOR and PI3K-Akt-mTOR pathways)...
September 2016: Cancer Treatment Reviews
Corinne De Laet
No abstract text is available yet for this article.
November 2016: Developmental Medicine and Child Neurology
Jing Yang, Fengyue Wang, Weiju Sun, Yanli Dong, Mingyu Li, Lu Fu
Despite the importance of testosterone as a metabolic hormone, its effects on myocardial metabolism in the ischemic heart remain unclear. Myocardial ischemia leads to metabolic remodeling, ultimately resulting in ATP deficiency and cardiac dysfunction. In the present study, the effects of testosterone replacement on the ischemic heart were assessed in a castrated rat myocardial infarction model established by ligating the left anterior descending coronary artery 2 weeks after castration. The results of real-time PCR and Western blot analyses showed that peroxisome proliferator-activated receptor α (PPARα) decreased in the ischemic myocardium of castrated rats, compared with the sham-castration group, and the mRNA expression of genes involved in fatty acid metabolism (the fatty acid translocase CD36, carnitine palmitoyltransferase I, and medium-chain acyl-CoA dehydrogenase) and glucose transporter-4 also decreased...
2016: PPAR Research
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