2018
DOI: 10.18632/aging.101577
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Abstract: A high-glucose diet (HGD) is associated with the development of metabolic diseases that decrease life expectancy, including obesity and type-2 diabetes (T2D); however, the mechanism through which a HGD does so is still unclear. Autophagy, an evolutionarily conserved mechanism, has been shown to promote both cell and organismal survival. The goal of this study was to determine whether exposure of Caenorhabditis elegans to a HGD affects autophagy and thus contributes to the observed lifespan reduction under a HG… Show more

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Cited by 13 publications
(11 citation statements)
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References 36 publications
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“…HLH-30 also contributes to longevity and survival through the brain–gut crosstalk, resulting in the higher expression of the detoxifying enzyme flavin-containing monooxygenase (FMO)-2 ( Leiser et al, 2015 ; Bennett et al, 2017 ) or ins-11, a neuropeptide that represses the aversion to pathogenic food ( Lee and Mylonakis, 2017 ). Notably, depending on the cellular context, HLH-30 may also induce cell death and shorten the life span, as was demonstrated in C. elegans exposed to a high-glucose diet ( Franco-Juarez et al, 2018 ). Although confirming this dual role in higher animals is a challenging task, the identification of genic counterparts and experiments in mammalian cells suggested that these mechanisms might be conserved ( Lapierre et al, 2013 ; Leiser et al, 2015 ; Lin et al, 2018 ; Silvestrini et al, 2018 ).…”
Section: Organism Development Longevity and Survival To Stressmentioning
confidence: 83%
“…HLH-30 also contributes to longevity and survival through the brain–gut crosstalk, resulting in the higher expression of the detoxifying enzyme flavin-containing monooxygenase (FMO)-2 ( Leiser et al, 2015 ; Bennett et al, 2017 ) or ins-11, a neuropeptide that represses the aversion to pathogenic food ( Lee and Mylonakis, 2017 ). Notably, depending on the cellular context, HLH-30 may also induce cell death and shorten the life span, as was demonstrated in C. elegans exposed to a high-glucose diet ( Franco-Juarez et al, 2018 ). Although confirming this dual role in higher animals is a challenging task, the identification of genic counterparts and experiments in mammalian cells suggested that these mechanisms might be conserved ( Lapierre et al, 2013 ; Leiser et al, 2015 ; Lin et al, 2018 ; Silvestrini et al, 2018 ).…”
Section: Organism Development Longevity and Survival To Stressmentioning
confidence: 83%
“…Consistent with this idea, Franco-Juarez et al exposed nematodes to a high-glucose diet and found that nematodes showed increased autophagic flux via an HLH-30/TFEB-dependent mechanism; however, their lifespan was diminished ( Figure 3 ). Since the nuclear localization of HLH-30/TFEB is dependent on its phosphorylation, they also treated worms with okadaic acid, an inhibitor of the PP2A and PP1 protein phosphatases, and found that this acid was capable of blocking the HLH-30/TFEB nuclear translocation during glucose exposure, suggesting that HLH-30/TFEB translocation is dependent on its phosphorylation status and might have detrimental effects on lifespan, possibly through autophagy under this stress condition [ 87 ]. In line with these outcomes, Mellor et al found that mice fed with a high fructose diet increase myocardial ROS production; moreover, they reported an increase in autophagy, perhaps as a consequence of elevated ROS, because ROS had been associated with induction of autophagy as part of the cell mechanism to protect cells from apoptosis.…”
Section: Impacts Of Carbohydrate Metabolism On Lifespanmentioning
confidence: 99%
“…Furthermore, in mouse models of obesity, suppression of TFEB, and Atg7 by liver-specific gene deletion facilitate liver steatosis and weight-gain ( Yang et al, 2010 ). Helix-Loop-Helix-30 (HLH-30), the TFEB ortholog as transcriptional switches, couple autophagy and lysosomal lipolysis to nutritional changes through mediating the efficient lipid clearance in Caenorhabditis Elegans, resulting in additive effects with controlling fat storage ( O’Rourke and Ruvkun, 2013 ; Franco-Juárez et al, 2018 ). In agreement with this, a similar conserved pathway is replicable in human cells ( Ji et al, 2020 ) and murine models ( Visvikis et al, 2014 ; Nakamura and Yoshimori, 2018 ), underscoring that HLH-30 or TFEB is conservative in linking autophagy to lipid homeostasis and lifespan.…”
Section: The Function and Molecular Mechanism Of Tfeb Regulating Lipimentioning
confidence: 99%