Can the beneficial effects of methionine restriction in rats be explained in part by decreased methylglyoxal generation resulting from suppressed carbohydrate metabolism?

Alan R. Hipkiss*

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

The mechanisms by which dietary restriction of the amino acid methionine exerts beneficial effects on oxidative damage towards rat liver mitochondria are discussed. It is suggested that methionine restriction decreases amino acid utilization in protein synthesis which, by decreasing synthesis of non-essential amino acids from carbohydrate precursors, also decreases formation of the highly deleterious glycolytic by-product methylglyoxal, a well-recognised source of age-related damage including formation of reactive oxygen species, mitochondrial dysfunction and proteotoxicity. Additionally, decreased protein synthesis will lower the error-protein load which the protein quality system (proteasomal and autophagic) must deal with to maintain proteostasis.

Original languageEnglish
Pages (from-to)633-636
Number of pages4
JournalBiogerontology
Volume13
Issue number6
Early online date23 Sep 2012
DOIs
Publication statusPublished - Dec 2012

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Pyruvaldehyde
Carbohydrate Metabolism
Methionine
Amino Acids
Proteins
Liver Mitochondrion
Reactive Oxygen Species
Carbohydrates

Keywords

  • dihydroxyacetone-phosphate
  • error-proteins
  • feedback control
  • fructose
  • glucose
  • glyceraldehyde-3-phosphate
  • glycolysis
  • glycoxidation
  • methylglyoxal
  • ROS
  • triosephosphate isomerase

Cite this

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title = "Can the beneficial effects of methionine restriction in rats be explained in part by decreased methylglyoxal generation resulting from suppressed carbohydrate metabolism?",
abstract = "The mechanisms by which dietary restriction of the amino acid methionine exerts beneficial effects on oxidative damage towards rat liver mitochondria are discussed. It is suggested that methionine restriction decreases amino acid utilization in protein synthesis which, by decreasing synthesis of non-essential amino acids from carbohydrate precursors, also decreases formation of the highly deleterious glycolytic by-product methylglyoxal, a well-recognised source of age-related damage including formation of reactive oxygen species, mitochondrial dysfunction and proteotoxicity. Additionally, decreased protein synthesis will lower the error-protein load which the protein quality system (proteasomal and autophagic) must deal with to maintain proteostasis.",
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T1 - Can the beneficial effects of methionine restriction in rats be explained in part by decreased methylglyoxal generation resulting from suppressed carbohydrate metabolism?

AU - Hipkiss, Alan R.

PY - 2012/12

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N2 - The mechanisms by which dietary restriction of the amino acid methionine exerts beneficial effects on oxidative damage towards rat liver mitochondria are discussed. It is suggested that methionine restriction decreases amino acid utilization in protein synthesis which, by decreasing synthesis of non-essential amino acids from carbohydrate precursors, also decreases formation of the highly deleterious glycolytic by-product methylglyoxal, a well-recognised source of age-related damage including formation of reactive oxygen species, mitochondrial dysfunction and proteotoxicity. Additionally, decreased protein synthesis will lower the error-protein load which the protein quality system (proteasomal and autophagic) must deal with to maintain proteostasis.

AB - The mechanisms by which dietary restriction of the amino acid methionine exerts beneficial effects on oxidative damage towards rat liver mitochondria are discussed. It is suggested that methionine restriction decreases amino acid utilization in protein synthesis which, by decreasing synthesis of non-essential amino acids from carbohydrate precursors, also decreases formation of the highly deleterious glycolytic by-product methylglyoxal, a well-recognised source of age-related damage including formation of reactive oxygen species, mitochondrial dysfunction and proteotoxicity. Additionally, decreased protein synthesis will lower the error-protein load which the protein quality system (proteasomal and autophagic) must deal with to maintain proteostasis.

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KW - error-proteins

KW - feedback control

KW - fructose

KW - glucose

KW - glyceraldehyde-3-phosphate

KW - glycolysis

KW - glycoxidation

KW - methylglyoxal

KW - ROS

KW - triosephosphate isomerase

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