Glucose delays age‐dependent proteotoxicity

Tauffenberger, Arnaud; Vaccaro, Alexandra; Aulas, Anaïs; Velde, Christine Vande; Parker, J. Alex

doi:10.1111/j.1474-9726.2012.00855.x

Cited by 42 publications

(57 citation statements)

References 41 publications

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“…It has previously been reported that sugar can have a detrimental effect on aging (Lee et al, 2009;Schlotterer et al, 2009;Schulz et al, 2007;Tauffenberger et al, 2012). Here, we have observed a similar detrimental effect at the higher concentrations tested (above 1% of glucose) and on non-proliferating E. coli.…”

Section: Mechanisms Ofsupporting

confidence: 75%

“…3A, Table S3). On the contrary, animals growing under this low concentration of sugar live shorter than those feeding on a sugar free medium, indicating a deleterious effect of the sugar for the longevity of the nematodes as has been described before (Lee et al, 2009;Schlotterer et al, 2009;Schulz et al, 2007;Tauffenberger et al, 2012) and here at higher concentration of sugars. Additionally, no increase in longevity is observed when animals fed UV-treated E. coli in the presence of 0.1% sugar (Supplementary data, Fig.…”

Section: Mechanisms Ofmentioning

confidence: 66%

“…Sugar is the preferred energy source for the cell, but despite its essential role for cell maintenance and growth, it has been demonstrated to accelerate aging, for instance glucose addition has been reported to shorten C. elegans life span (Lee et al, 2009;Schlotterer et al, 2009;Schulz et al, 2007;Tauffenberger et al, 2012). The standard method to culture C. elegans consists in growing the nematodes on agar plates without sugar containing a lawn of living OP50 strain of E. coli (Brenner, 1974).…”

mentioning

confidence: 99%

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Escherichia coli carbon source metabolism affects longevity of its predator Caenorhabditis elegans

Brokate-Llanos

Garzón

Muñoz

2014

Mechanisms of Ageing and Development

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Section: Mechanisms Ofsupporting

confidence: 75%

Section: Mechanisms Ofmentioning

confidence: 66%

mentioning

confidence: 99%

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Escherichia coli carbon source metabolism affects longevity of its predator Caenorhabditis elegans

Brokate-Llanos

Garzón

Muñoz

2014

Mechanisms of Ageing and Development

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“…Surprisingly, CaI reduced oligomerization of Aβ in control worms that expressed Aβ, but in which the dld-1 gene was not suppressed by RNAi. Matching results were also reported by Tauffenberger et al [506] where high glucose concentrations protect against Aβ-mediated paralysis but simultaneously induced the formation of toxic oligomers of Aβ. Overall, the protective effect of MICA seems to occur through inhibition of Aβ oligomerization, which can be modulated through calcium signaling.…”

Section: Discussionsupporting

confidence: 88%

“…We found that either 1% glucose or 1% glycerol alleviated paralysis in Aβ transgenic worms. Tauffenberger et al [506] previously found the same result for glucose in worms and suggested that glucose enrichment protects against Aβ proteotoxicity and neurodegeneration. Our results are consistent with this interpretation for both glucose and glycerol.…”

Section: Discussionsupporting

confidence: 54%

Metabolic study of Alzheimer’s disease using mutant C. elegans

Ahmad¹

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Alzheimer's disease (AD) is associated with chronic neurodegeneration and is the cause of the most common form of dementia. The main hallmarks of AD are aggregates of amyloid beta (Aβ) and formation of hyperphosphorylated tau neurofibrillary tangles (NFTs). Unfortunately, after more than 100 years of research the exact cause(s) and mechanisms involved in AD progression remain unclarified. Evidence indicates that impaired mitochondrial bioenergetics may precede by decades, the neurodegeneration and cognitive decline associated with AD. Moreover, a genetic association of the core metabolic enzyme dihydrolipoamide dehydrogenase (DLD) with late-onset AD and reduced activity of DLD-containing enzymes suggests glucose hypo-metabolism as a possible cause of AD. Contrary to this, improvements of AD symptoms under caloric restriction or other means of reducing-glucose dependent energy metabolism supports an alternative hypothesis that a decrease in glucose metabolism may be protective. In the present study, we used mutant Caenorhabditis elegans (C. elegans) to investigate the effect of glucose metabolism on AD progression. We initially looked at the role of suppressed DLD-1, and then we focused on the effect of high glucose in AD pathogenesis.Transgenic expression of Aβ in C. elegans causes both phenotypic and behavioral defects and results in accumulation of toxic Aβ oligomers, culminating in protein aggregation as is normally associated with AD pathophysiology. Aβ expression in worm muscle causes agedependent progressive paralysis and impaired acetylcholine neurotransmission while neuronal Aβ expression results in defective chemotaxis and impaired serotonin sensitivity as well as reduced fecundity and egg hatching. Suppression of the dld-1 gene alleviated paralysis, improved acetylcholine neurotransmission, enhanced chemotaxis and restored normal sensitivity to serotonin.dld-1 gene suppression also protects vitality as indicated by improved fecundity and egg hatching.Interestingly, protective effects of dld-1 suppression could be reversed using the calcium ionophore (CaI), indicating that the protective mechanism involves calcium signaling. Each of these beneficial effects of dld-1 gene suppression could be mimicked using a specific, small molecule inhibitor of the DLD-1 enzyme, 5-methoxyindole-2-carboxylic acid (MICA).High glucose levels are associated with the metabolic disorder, diabetes, which is a major risk factor for AD. In fact, it has been suggested that AD is a neural form of diabetes, type 3 diabetes. If true, drugs used to treat diabetes could act as possible treatments for AD. In this study, I investigated the effect of elevated glucose, the glucose metabolism inhibitor, 2-deoxy-d-glucose ii (2DOG) as well as the anti-diabetes drugs, metformin and 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), on AD progression. Elevated glucose in the growth medium induced hyperactivity, which interfered with the paralysis assays, but it was seen to impair cholinergic neurotransmission, egg laying and hatc...

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Higher Glycemic Index and Glycemic Load Diet Is Associated with Slower Disease Progression in Amyotrophic Lateral Sclerosis

Lee,

Mitsumoto,

Lee

et al. 2023

Annals of Neurology

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ObjectiveHigh‐caloric diets may slow the progression of amyotrophic lateral sclerosis; however, key macronutrients have not been identified. We examined whether dietary macronutrients are associated with the rate of progression and length of survival among the prospective cohort study participants.MethodsParticipants with a confirmed diagnosis of sporadic amyotrophic lateral sclerosis enrolled in the Multicenter Cohort Study of Oxidative Stress were included (n=304). We evaluated baseline macronutrient intake assessed by food frequency questionnaire in relation to change in revised amyotrophic lateral sclerosis functional rating scale total‐score, and tracheostomy‐free survival using linear regression and Cox proportional hazard models. Baseline age, sex, disease duration, diagnostic certainty, body mass index, bulbar onset, revised amyotrophic lateral sclerosis functional rating scale total‐score, and forced vital capacity were included as covariates.ResultsBaseline higher glycemic index and load were associated with less decline of revised amyotrophic lateral sclerosis functional rating scale total‐score at 3‐month follow‐up (β= ‐0.13, 95% Confidence Interval [‐0.2, ‐0.01], p=0.03) and (β= ‐0.01, [‐0.03, ‐0.0007], p=0.04) respectively. Glycemic index second‐quartile, third‐quartile, and fourth‐quartile groups were associated with less decline at 3‐month by 1.9 ([‐3.3, ‐0.5], p=0.008), 2.0 ([‐3.3, ‐0.6], p=0.006), and 1.6 ([‐3.0, ‐0.2], p=0.03) points compared to the first‐quartile group; glycemic load fourth‐quartile group had 1.4 points less decline compared to the first‐quartile group ([‐2.8, 0.1], p=0.07). Higher glycemic index was associated with a trend toward longer tracheostomy‐free survival (Hazard ratio 0.97, [0.93, 1.00], p=0.07).InterpretationHigher dietary glycemic index and load are associated with slower disease progression in amyotrophic lateral sclerosis.This article is protected by copyright. All rights reserved.

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Glucose delays age‐dependent proteotoxicity

Cited by 42 publications

References 41 publications

Escherichia coli carbon source metabolism affects longevity of its predator Caenorhabditis elegans

Escherichia coli carbon source metabolism affects longevity of its predator Caenorhabditis elegans

Metabolic study of Alzheimer’s disease using mutant C. elegans

Higher Glycemic Index and Glycemic Load Diet Is Associated with Slower Disease Progression in Amyotrophic Lateral Sclerosis

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