mTOR signaling in cellular and organismal energetics
Abstract
Mammalian TOR (mTOR) signaling controls growth, metabolism and energy homeostasis in a cell autonomous manner. Recent findings indicate that mTOR signaling in one tissue can also affect other organs thereby affecting whole body metabolism and energy homeostasis in a non-cell autonomous manner. It is thus not surprising that mTOR signaling mediates aging and is often deregulated in metabolic disorders, such as obesity, diabetes and cancer. This review discusses the regulation of cellular and whole body energy metabolism by mTOR, with particular focus on the non-cell autonomous function of mTOR.
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mTOR signaling is dysregulated in cancer, T2DM and obesity, and is therefore actively pursued as a promising drug target.
“Indeed, mTOR signaling is dysregulated in cancer, T2DM and obesity, and is therefore actively perused as a promising drug target [reviewed in Laplante and Sabatini (275 and Albert and Hall (278)].”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [278]
Increased mTOR signaling in either adipose tissue, skeletal muscle, or the liver negatively affects systemic glucose and insulin homeostasis.
“For instance, increased mTOR signaling in either adipose tissue, skeletal muscle, or the liver, negatively affects systemic glucose and insulin homeostasis (278).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [278]
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- Authors
- Albert, V., & Hall, M. N.
- Affiliations
- University of Basel (CH)
- Corresponding author
- Hall, Michael N
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 33
- Pages
- 55-66
- ISSN
- 0955-0674 (ISSN-L)
- OpenAlex
- W2065952016
- Cited by
- 304
- References
- 92
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 7 · 2023: 17 · 2022: 29 · 2021: 43 · 2020: 19 · 2019: 26 · 2018: 24 · 2017: 41 · 2016: 58 · 2015: 23
- FWCI
- 3.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Swiss National Science Foundation (Loius-Jeantet Foundation, European Research Council, Werner Siemens Foundation (VA), Canton of Basel-Stadt)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mTOR signaling, energy homeostasis, whole-body metabolism, non-cell-autonomous signaling, aging, obesity, diabetes mellitus, cancer
- MeSH terms
- Adipose Tissue, Animals, Energy Metabolism, Homeostasis, Humans, Hypothalamus, Liver, Metabolic Diseases, Mitochondria, Nucleotides, Protein Biosynthesis, Signal Transduction, Muscle, Skeletal, TOR Serine-Threonine Kinases
About these checks
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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