A high glucose diet induces autophagy in a HLH-30/TFEB-dependent manner and impairs the normal lifespan of C. elegans

Franco-Juárez, Berenice; Mejia-Martinez, Fanny; Moreno-Arriola, Elizabeth; Hernandez-Vazquez, Alain de J.; Gómez-Manzo, Saúl; Marcial-Quino, Jaime; Arreguín-Espinosa, Roberto; Velázquez-Arellano, Antonio; Ortega-Cuellar, Daniel

doi:10.18632/aging.101577

Cited by 13 publications

(11 citation statements)

References 36 publications

(47 reference statements)

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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%

MiT/TFE Family of Transcription Factors: An Evolutionary Perspective

Spina

Contreras

Rissone

et al. 2021

Front. Cell Dev. Biol.

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Graphical AbstractMiT/TFE transcription factors are master regulators of cellular adaptation to a wide variety of stressful conditions. They control the expression of a plethora of genes involved in response to nutrient deprivation, oxidative and ER stress, and DNA and mitochondrial damage. MiT/TFE proteins play a critical role in organelle biogenesis, control of energy homeostasis, adaptation to pathogen infection, control of growth and development, aging, and death. MiT/TFE proteins are also modulators of critical signaling pathways that regulate cell proliferation, cellular fate commitment, and tumorigenesis. Many of these functions are evolutionary conserved from lower metazoans to mammals indicating that the adaptation to challenging conditions occurred early during evolution.

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Section: Organism Development Longevity and Survival To Stressmentioning

confidence: 83%

MiT/TFE Family of Transcription Factors: An Evolutionary Perspective

Spina

Contreras

Rissone

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Buy / Rent full text

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“…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%

TFEB: A Emerging Regulator in Lipid Homeostasis for Atherosclerosis

Wang

et al. 2021

Front. Physiol.

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Atherosclerosis, predominantly characterized by the disturbance of lipid homeostasis, has become the main causation of various cardiovascular diseases. Therefore, there is an urgent requirement to explore efficacious targets that act as lipid modulators for atherosclerosis. Transcription factor EB (TFEB), whose activity depends on post-translational modifications, such as phosphorylation, acetylation, SUMOylation, ubiquitination, etc., is significant for normal cell physiology. Recently, increasing evidence implicates a role of TFEB in lipid homeostasis, via its functionality of promoting lipid degradation and efflux through mediating lipophagy, lipolysis, and lipid metabolism-related genes. Furthermore, a regulatory effect on lipid transporters and lipid mediators by TFEB is emerging. Notably, TFEB makes a possible therapeutic target of atherosclerosis by regulating lipid metabolism. This review recapitulates the update and current advances on TFEB mediating lipid metabolism to focus on two intracellular activities: a) how cells perceive external stimuli and initiate transcription programs to modulate TFEB function, and b) how TFEB restores lipid homeostasis in the atherosclerotic process. In-depth research is warranted to develop potent agents against TFEB to alleviate or reverse the progression of atherosclerosis.

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“…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%

Effects of High Dietary Carbohydrate and Lipid Intake on the Lifespan of C. elegans

Franco-Juárez

Gómez-Manzo²,

Hernández-Ochoa³

et al. 2021

Cells

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Health and lifespan are influenced by dietary nutrients, whose balance is dependent on the supply or demand of each organism. Many studies have shown that an increased carbohydrate–lipid intake plays a critical role in metabolic dysregulation, which impacts longevity. Caenorhabditis elegans has been successfully used as an in vivo model to study the effects of several factors, such as genetic, environmental, diet, and lifestyle factors, on the molecular mechanisms that have been linked to healthspan, lifespan, and the aging process. There is evidence showing the causative effects of high glucose on lifespan in different diabetic models; however, the precise biological mechanisms affected by dietary nutrients, specifically carbohydrates and lipids, as well as their links with lifespan and longevity, remain unknown. Here, we provide an overview of the deleterious effects caused by high-carbohydrate and high-lipid diets, as well as the molecular signals that affect the lifespan of C. elegans; thus, understanding the detailed molecular mechanisms of high-glucose- and lipid-induced changes in whole organisms would allow the targeting of key regulatory factors to ameliorate metabolic disorders and age-related diseases.

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A high glucose diet induces autophagy in a HLH-30/TFEB-dependent manner and impairs the normal lifespan of C. elegans

Cited by 13 publications

References 36 publications

MiT/TFE Family of Transcription Factors: An Evolutionary Perspective

MiT/TFE Family of Transcription Factors: An Evolutionary Perspective

TFEB: A Emerging Regulator in Lipid Homeostasis for Atherosclerosis

Effects of High Dietary Carbohydrate and Lipid Intake on the Lifespan of C. elegans

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