Molecular mechanisms linking calorie restriction and longevity
Abstract
Calorie-restricted feeding retards the rate of ageing in mammalian and invertebrate species. The molecular mechanisms underlying this effect include a lower rate of accrual of tissue oxidative damage that is associated with a significantly lower rate of mitochondrial free radical generation in rodent species. To identify the important sites of control and regulation for mitochondrial free radical generation during ageing and calorie-restricted feeding, metabolic control analysis is being applied to the study of mitochondrial bioenergetics. With ageing an increase in the mitochondrial proton leak is observed in mouse hepatocytes and in rat skeletal muscle. Limited data suggest that calorie-restricted feeding lowers the inner mitochondrial membrane potential and this may explain the reduced rate of free radical generation. A lowered unsaturation/saturation index is observed for mitochondrial membrane lipids in calorie-restricted rodents resulting in an altered membrane structure and function. Plasma concentrations of insulin and triiodothyronine are significantly lower under calorie-restricted feeding conditions and these hormones exert transcriptional control over desaturase enzymes that are important in the control of membrane lipid unsaturation. A loss of double bonds should make the mitochondrial membranes more resistant to peroxidation damage and would also reduce the proton conductance of the membrane, raising the membrane potential at a given respiration rate. This effect however, appears to be offset by other membrane changes that may include increased activity of uncoupling proteins. These unidentified adaptations increase the proton leak in calorie-restricted animals resulting in a lowering of the membrane potential and ROS generation.
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Ageing is associated with accumulation of deficient mitochondria that produce a significant increase of ROS generation.
“Some evidence indicate that ageing is associated with the accumulation of deficient mitochondria that produce a significant increase of ROS generation (Chistiakov et al., 2014; Merry, 2002).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Merry, 2002
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- Authors
- Merry, B. J.
- Affiliations
- University of Liverpool (GB)
- Corresponding author
- Merry, B.J
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2002-11
- Volume
- 34
- Issue
- 11
- Pages
- 1340-1354
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W2016797892
- Cited by
- 304
- References
- 91
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 10 · 2022: 4 · 2021: 6 · 2020: 10 · 2019: 6 · 2018: 6 · 2017: 14 · 2016: 10 · 2015: 11 · 2014: 21 · 2013: 13 · 2012: 10
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- caloric restriction, longevity, aging, oxidative damage, mitochondrial proton leak, mitochondrial membrane potential, membrane lipid unsaturation, desaturase enzymes, insulin, triiodothyronine, uncoupling proteins, metabolic control analysis, hepatocytes, skeletal muscle
- MeSH terms
- Uncoupling Protein 3, Animals, Carrier Proteins, Cell Membrane, Hormones, Humans, Invertebrates, Ion Channels, Longevity, Mitochondria, Statistics as Topic, Uncoupling Agents, Reactive Oxygen Species, Oxidative Stress, Mitochondrial Proteins, Caloric Restriction
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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