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Plos One : Fgt-1 is a Mammalian Glut2-like Facilitative Glucose Transporter in Caenorhabditis Elegans Whose Malfunction Induces Fat Accumulation in Intestinal Cells, Volume 8

By Lamitina, Todd

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Book Id: WPLBN0003948494
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Reproduction Date: 2015

Title: Plos One : Fgt-1 is a Mammalian Glut2-like Facilitative Glucose Transporter in Caenorhabditis Elegans Whose Malfunction Induces Fat Accumulation in Intestinal Cells, Volume 8  
Author: Lamitina, Todd
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
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Publisher: Plos

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Lamitina, T. (n.d.). Plos One : Fgt-1 is a Mammalian Glut2-like Facilitative Glucose Transporter in Caenorhabditis Elegans Whose Malfunction Induces Fat Accumulation in Intestinal Cells, Volume 8. Retrieved from http://netlibrary.net/


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Description : Caenorhabditis elegans (C. elegans) is an attractive animal model for biological and biomedical research because it permits relatively easy genetic dissection of cellular pathways, including insulin/IGF-like signaling (IIS), that are conserved in mammalian cells. To explore C. elegans as a model system to study the regulation of the facilitative glucose transporter (GLUT), we have characterized the GLUT gene homologues in C. elegans : fgt-1, R09B5.11, C35A11.4, F53H8.3, F48E3.2, F13B12.2, Y61A9LA.1, K08F9.1 and Y37A1A.3. The exogenous expression of these gene products in Xenopus oocytes showed transport activity to unmetabolized glucose analogue 2-deoxy-D-glucose only in FGT-1. The FGT-1-mediated transport activity was inhibited by the specific GLUT inhibitor phloretin and exhibited a Michaelis constant (Km) of 2.8 mM. Mannose, galactose, and fructose were able to inhibit FGT-1- mediated 2-deoxy-D-glucose uptake (P < 0.01), indicating that FGT-1 is also able to transport these hexose sugars. A GFP fusion protein of FGT-1 was observed only on the basolateral membrane of digestive tract epithelia in C. elegans, but not in other tissues. FGT-1::eGFP expression was observed from early embryonic stages. The knockdown or mutation of fgt-1 resulted in increased fat staining in both wild-type and daf-2 (mammalian insulin receptor homologue) mutant animals. Other common phenotypes of IIS mutant animals, including dauer formation and brood size reduction, were not affected by fgt-1 knockdown in wild-type or daf-2 mutants. Our results indicated that in C. elegans, FGT-1 is mainly a mammalian GLUT2-like intestinal glucose transporter and is involved in lipid metabolism.

 

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