Fasting: molecular mechanisms and clinical applications
Open accessAbstract
Fasting has been practiced for millennia, but, only recently, studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism, and bolster cellular protection. In lower eukaryotes, chronic fasting extends longevity, in part, by reprogramming metabolic and stress resistance pathways. In rodents intermittent or periodic fasting protects against diabetes, cancers, heart disease, and neurodegeneration, while in humans it helps reduce obesity, hypertension, asthma, and rheumatoid arthritis. Thus, fasting has the potential to delay aging and help prevent and treat diseases while minimizing the side effects caused by chronic dietary interventions.
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During fasting, the decrease in circulating dietary carbohydrates and lipids and decline in insulin-glucagon ratio induces a switch toward fatty acid oxidation.
“During fasting, the decrease in circulating dietary carbohydrates and lipids and decline in insulin-glucagon ratio induces a switch toward FAO (20).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [20]
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- Authors
- Longo, V. D., & Mattson, M. P.
- Affiliations
- University of Southern California (US)
- National Institutes of Health (US)
- Corresponding author
- Longo, Valter D.
- Mattson, Mark P.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-02
- Volume
- 19
- Issue
- 2
- Pages
- 181-192
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC3946160
- OpenAlex
- W2129132663
- Cited by
- 1,425
- References
- 111
- Citations by year
- 2026: 100 · 2025: 138 · 2024: 132 · 2023: 131 · 2022: 148 · 2021: 163 · 2020: 168 · 2019: 93 · 2018: 119 · 2017: 87 · 2016: 69 · 2015: 55 · 2014: 20
- FWCI
- 9.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Glenn Foundation for Medical Research
- National Institutes of Health
- National Institute on Aging (P01AG034906, ZIAAG000314, AG20642, ZIAAG000331, R01AG020642, ZIAAG000312, AG034906, AG025135, ZIAAG000315, R01AG025135)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK079637)
- Topics
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- fasting, intermittent fasting, cellular stress response, oxidative damage, inflammation, energy metabolism, longevity, disease prevention, obesity, aging, neurodegeneration, diabetes mellitus, cancer
- MeSH terms
- Animals, Fasting, Heart Diseases, Humans, Inflammation, Oxidative Stress, Mice, Rats
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