Muscle ectopic fat deposition contributes to anabolic resistance in obese sarcopenic old rats through e IF 2α activation
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Summary: Obesity and aging are characterized by decreased insulin sensitivity (IS) and muscle protein synthesis. Intramuscular ceramide accumulation has been implicated in insulin resistance during obesity. We aimed to measure IS, muscle ceramide level, protein synthesis, and activation of intracellular signaling pathways involved in translation initiation in male Wistar young (YR, 6‐month) and old (OR, 25‐month) rats receiving a low‐ (LFD) or a high‐fat diet (HFD) for 10 weeks. A corresponding cellular approach using C2C12 myotubes treated with palmitate to induce intracellular ceramide deposition was taken. A decreased ability of adipose tissue to store lipids together with a reduced adipocyte diameter and a development of fibrosis were observed in OR after the HFD. Consequently, OR fed the HFD were insulin resistant, showed a strong increase in intramuscular ceramide level and a decrease in muscle protein synthesis associated with increased eIF2α phosphorylation. The accumulation of intramuscular lipids placed a lipid burden on mitochondria and created a disconnect between metabolic and regulating pathways in skeletal muscles of OR. In C2C12 cells, palmitate‐induced ceramide accumulation was associated with a decreased protein synthesis together with upregulated eIF2α phosphorylation. In conclusion, a reduced ability to expand adipose tissues was found in OR, reflecting a lower lipid buffering capacity. Muscle mitochondrial activity was affected in OR conferring a reduced ability to oxidize fatty acids entering the muscle cell. Hence, OR were more prone to ectopic muscle lipid accumulation than YR, leading to decreased muscle protein anabolism. This metabolic change is a potential therapeutic target to counter sarcopenic obesity.
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Discrepancies in muscle mass and function may be due, at least in part, to current methodological limitations in accurate assessment of skeletal muscle mass.
“Discrepancies in muscle mass and function may be also due, at least in part, to current methodological limitations in accurate assessment of skeletal muscle mass (86).”
From Definition and diagnostic criteria for sarcopenic obesity: ESPEN and EASO consensus statement (2022) · cites this paper as [86]
The Discussion describes limitations in immunohistochemistry and possible differences in the rats’ physical activity, but does not discuss limitations in accurately assessing skeletal muscle mass. The Results report changes in hindlimb muscle weight; neither those passages nor searches for assessment limitations and mass–function discrepancies address the claimed explanation. (LLM, conf=0.73)
Experimental — accuracy not yet measuredThe synergy between muscle loss and fatty infiltration might trigger and aggravate the pathogenesis of sarcopenic obesity (SO).
“This synergy between muscle loss and fatty infiltration might trigger and aggravate the pathogenesis of sarcopenic obesity (SO).[ 13 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [13]
One of the major mechanisms that cause muscle IR is thought to be the myocytes' accumulation of secondary products of lipid metabolism such as DAG, ceramides, and other lipids in IMCLs.
“One of the major mechanisms that cause muscle IR is thought to be the myocytes' accumulation of secondary products of lipid metabolism such as DAG, ceramides, and other lipids in IMCLs.[ 13 ]”
From Pathogenesis of sarcopenia and the relationship with fat mass: descriptive review (2022) · cites this paper as [13]
Near-normal skeletal muscle mass according to reference ranges for the general non-obese population may be accompanied by lower or inadequate muscle strength and performance in individuals with obesity.
“However, near-normal skeletal muscle mass according to reference ranges for the general non-obese population may be accompanied by lower or inadequate muscle strength and performance in individuals with obesity [82].”
From Definition and Diagnostic Criteria for Sarcopenic Obesity: ESPEN and EASO Consensus Statement (2022) · cites this paper as [82]
Age, ethnicity and specific disease conditions may require specific equations and cut-offs that may not be available for different devices.
“Also, age, ethnicity and specific disease conditions may require specific equations and cut-offs [82] that may not be available for different devices.”
From Definition and Diagnostic Criteria for Sarcopenic Obesity: ESPEN and EASO Consensus Statement (2022) · cites this paper as [82]
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- Authors
- Tardif, N., Salles, J., Guillet, C., Tordjman, J., Reggio, S., Landrier, J., Giraudet, C., Patrac, V., Bertrand‐Michel, J., Migne, C., Collin, M., Chardigny, J., Boirie, Y., & Walrand, S.
- Affiliations
- Université Clermont Auvergne (FR)
- Inserm (FR)
- Institut National de la Recherche Agronomique (FR)
- Clermont Université Université d'Auvergne Unité de Nutrition Humaine BP 10448 Clermont‐Ferrand F‐63000 France
- Corresponding author
- Walrand, Stéphane
- ORCID
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2014-08-19
- Volume
- 13
- Issue
- 6
- Pages
- 1001-1011
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC4326920
- OpenAlex
- W2170351370
- Cited by
- 186
- References
- 56
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 16 · 2023: 20 · 2022: 21 · 2021: 18 · 2020: 17 · 2019: 15 · 2018: 14 · 2017: 12 · 2016: 18 · 2015: 10 · 2014: 1
- FWCI
- 6.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Agence National pour la Recherche (LIPAGE)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- sarcopenic obesity, ectopic fat deposition, eIF2α phosphorylation, insulin resistance, muscle protein synthesis, aging, high-fat diet, adipose tissue fibrosis, mitochondrial dysfunction, fatty acid oxidation, translation initiation, palmitate, C2C12 myotubes
- MeSH terms
- Adipose Tissue, Aging, Animals, Ceramides, Disease Models, Animal, Insulin Resistance, Male, Obesity, Signal Transduction, Eukaryotic Initiation Factor-2, Rats, Wistar, Muscle, Skeletal, eIF-2 Kinase, Rats, Sarcopenia, Diet, High-Fat
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