Oncotarget: Caloric restriction creates a metabolic pattern of chronological aging delay 熱量限制會產生按時間順序延緩衰老的新陳代謝模式

News Release 17-May-2021

Editor’s note: Again that is why eating less can delay or slow down the aging process. Eating less or caloric restriction can prevent and or treat disease like cancer which makes sense. Because if you slow the aging process, you are more likely to live longer. If you can live longer, then it means that you are less likely to have diseases (which would lead to premature death.) So if you want, you may start eating less. But it is not easy to restrict your caloric intake. You need to strategy. Particularly, those who have some health conditions already should think hard to figure out why they get this or that disease.

編者註:這又是為什麼少吃會延遲或延緩衰老過程的原因。 少吃或限制熱量可以預防和/或治療有意義的疾病,例如癌症。 因為如果您延緩衰老過程,則您更有可能活得更長壽。 如果壽命更長,則意味著您患疾病的可能性較小(這將導致過早死亡。)因此,如果您願意,則可以開始減少進食。 但是限制熱量的攝入並不容易。 您需要製定策略。 特別是,那些已經有些健康狀況的人應該認真思考以找出為什麼會患上這種疾病。

The Oncotarget authors propose a model of how the specific remodeling of cellular metabolism by caloric restriction contributes to yeast chronological aging delay.

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IMAGE: A hypothetical model of how a specific remodeling of cellular metabolism by CR slows down yeast chronological aging. See the text for more details. Abbreviations: Cys, cysteine; Met, methionine; Ppa2p,… view more  Credit: Correspondence to – Vladimir I. Titorenko – [email protected]

The cover for issue 7 of Oncotarget features Figure 14, “A hypothetical model of how a specific remodeling of cellular metabolism by CR slows down yeast chronological aging,” published in “Caloric restriction creates a metabolic pattern of chronological aging delay that in budding yeast differs from the metabolic design established by two other geroprotectors” by Mohammad, et al. which reported that caloric restriction and the tor1Δ mutation are robust geroprotectors in yeast and other eukaryotes.

The authors demonstrate that caloric restriction generates a unique metabolic pattern.

Unlike the tor1Δ mutation or lithocholic acid, it slows down the metabolic pathway for sulfur amino acid biosynthesis from aspartate, sulfate and 5-methyltetrahydrofolate.

Consequently, caloric restriction significantly lowers the intracellular concentrations of methionine, S-adenosylmethionine and cysteine.

They also noticed that the low-calorie diet, but not the tor1Δ mutation or lithocholic acid, decreases intracellular ATP, increases the ADP:ATP and AMP:ATP ratios, and rises intracellular ADP during chronological aging. The Oncotarget authors propose a model of how the specific remodeling of cellular metabolism by caloric restriction contributes to yeast chronological aging delay.

The Oncotarget authors propose a model of how the specific remodeling of cellular metabolism by caloric restriction contributes to yeast chronological aging delay.

Dr. Vladimir I. Titorenko from Concordia University said, “A body of evidence indicates that metabolism is an essential contributor to the aging and longevity of eukaryotic organisms across phyla.

Indeed, healthy aging of the evolutionarily distant eukaryotes coincides with age-related changes in the concentrations of specific metabolites within cells, tissues, organs and biological fluids.

Furthermore, such dietary interventions as caloric restriction, reduced protein intake, a limited supply of single amino acid and alternating cycles of feeding and fasting are robust geroprotectors that specifically rewire cellular and organismal metabolism in various eukaryotic organisms.

Moreover, allelic variants of the genes implicated in diverse metabolic pathways delay aging and extend longevity in eukaryotic organisms across species.

Besides, pharmacological interventions that target distinct aspects of metabolism are potent geroprotectors in diverse eukaryotes; these interventions include metformin, rapamycin, resveratrol, spermidine and others.

It remains unclear if different dietary, genetic and pharmacological anti-aging interventions set up a similar metabolic pattern of aging delay or each of them generates a distinct metabolic profile.

The Titorenko Research Team concluded in their Oncotarget Research Output that:

1. What is the mechanism responsible for ATP decline under CR conditions? They hypothesize that CR might affect the transcription and/or translation of enzymes involved in ATP synthesis and/or degradation in the cytosol, mitochondria or other cellular locations.

Of note, a transcription/translation-based mechanism of suppressing methionine biosynthetic enzymes and transporters underlies the ability of CR to lower intracellular methionine and extend yeast RLS.

2. What are the metabolic changes underlying the extremely efficient longevity extension in yeast culture under CR conditions with LCA? Their findings indicate that LCA applied under CR conditions “overrides” the CR-specific metabolic profile of aging delay.

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DOIhttps://doi.org/10.18632/oncotarget.27926

Full texthttps://www.oncotarget.com/article/27926/text/

Correspondence to – Vladimir I. Titorenko – [email protected]

Keywords cellular aging, geroprotectors, caloric restriction, metabolism, methionine

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