Journal
BIOCHEMICAL JOURNAL
Volume 456, Issue -, Pages 219-229Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20131101
Keywords
aging; Caenorhabditis elegans; facilitated glucose transporter; isoform 1 (fgt-1); glucose transport; insulin; metabolism
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Funding
- Medical Research Council (U.K.) [MR/G9225018, MR/J003417/1]
- University of Georgia, College of Veterinary Medicine
- British Heart Foundation [PG/11/52/28989] Funding Source: researchfish
- Medical Research Council [MR/J003417/1, G0300415, G9225018] Funding Source: researchfish
- MRC [G9225018, MR/J003417/1, G0300415] Funding Source: UKRI
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Caenorhabditis elegans is widely used as a model for investigation of the relationships between aging, nutrient restriction and signalling via the DAF-2 (abnormal dauer formation 2) receptor for insulin-like peptides and AGE-1 [ageing alteration 1; orthologue of PI3K (phosphoinositide 3-kinase)], but the identity of the glucose transporters that may link these processes is unknown. We unexpectedly find that of the eight putative GLUT (glucose transporter)-like genes only the two splice variants of one gene have a glucose transport function in an oocyte expression system. We have named this gene fgt-1 (facilitated glucose transporter, isoform 1). We show that knockdown of fgt-1 RNA leads to loss of glucose transport and reduced glucose metabolism in wild-type worms. The FGT-1 glucose transporters of C. elegans thus play a key role in glucose energy supply to C. elegans. Importantly, knockdown of fgt-1 leads to an extension of lifespan equivalent, but not additive, to that observed in daf-2 and age-1 mutant worms. The results of the present study are consistent with DAF-2 and AGE-1 signalling stimulating glucose transport in C. elegans and this process being associated with the longevity phenotype in daf-2 and age-1 mutant worms. We propose that fgt-1 constitutes a common axis for the lifespan extending effects of nutrient restriction and reduced insulin-like peptide signalling.
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