Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility
Open accessAbstract
The ability of skeletal muscle to switch between lipid and glucose oxidation for ATP production during metabolic stress is pivotal for maintaining systemic energy homeostasis, and dysregulation of this metabolic flexibility is a dominant cause of several metabolic disorders. However, the molecular mechanism that governs fuel selection in muscle is not well understood. Here, we report that brain-derived neurotrophic factor (BDNF) is a fasting-induced myokine that controls metabolic reprograming through the AMPK/CREB/PGC-1α pathway in female mice. Female mice with a muscle-specific deficiency in BDNF (MBKO mice) were unable to switch the predominant fuel source from carbohydrates to fatty acids during fasting, which reduced ATP production in muscle. Fasting-induced muscle atrophy was also compromised in female MBKO mice, likely a result of autophagy inhibition. These mutant mice displayed myofiber necrosis, weaker muscle strength, reduced locomotion, and muscle-specific insulin resistance. Together, our results show that muscle-derived BDNF facilitates metabolic adaption during nutrient scarcity in a gender-specific manner and that insufficient BDNF production in skeletal muscle promotes the development of metabolic myopathies and insulin resistance.
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BDNF promotes mitochondrial transport of fatty acids and expression of genes related to fatty acid oxidation by activating AMPK, PPARα, Nur77, and PGC-1α pathways.
“BDNF promotes the mitochondrial transport of fatty acids and the expression of genes related to FAO by activating the AMPK, PPARα, Nur77, and PGC-1α pathways [109].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [109]
Disruption of these signaling pathways in muscle with muscle-specific BDNF knockout leads to reduced ATP production through FAO and diminished amino acid release from fasting-induced autophagy, resulting in myofiber necrosis.
“Since these signaling pathways are also critical for mitochondrial biogenesis and autophagy during fasting, their disruption in muscle with muscle-specific BDNF knockout leads to a reduction in ATP production through FAO, as well as diminished amino acid release from fasting-induced autophagy, resulting in myofiber necrosis [109].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [109]
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- Authors
- Yang, X., Brobst, D., Chan, W. S., Tse, M. C. L., Herlea-Pana, O., Ahuja, P., Bi, X., Zaw, A. M., Kwong, Z. S. W., Jia, W.-H., Zhang, Z.-G., Zhang, N., Chow, S. K. H., Cheung, W. H., Louie, J. C. Y., Griffin, T. M., Nong, W., Hui, J. H. L., Du, G.-H., Noh, H. L., Saengnipanthkul, S., Chow, B. K. C., Kim, J. K., Lee, C. W., & Chan, C. B.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- University of Oklahoma Health Sciences Center (US)
- University of Hong Kong (HK)
- Department of Physiology, University of Oklahoma Health Sciences Center, 940 Stanton L. Young Blvd., BMSB 634, Oklahoma City, OK 73104, USA.
- University of Waterloo (CA)
- State Key Laboratory of Bioactive Substance and Function of Natural Medicines and Beijing Key Laboratory of Drug Target and Screening Research, Institute of Materia Medica of Peking Union Medical College, Beijing 100050, China.
- Liaoning Cancer Hospital & Institute (CN)
- Chinese University of Hong Kong (HK)
- Oklahoma Medical Research Foundation (US)
- University of Massachusetts Chan Medical School (US)
- School of Biological Sciences, The University of Hong Kong, 6N01 Kadoorie Biological Sciences Building, Pokfulam Road, Hong Kong.
- Corresponding author
- Yang, Xiuying
- Brobst, Daniel
- Lee, Chi Wai
- Chan, Chi Bun
- ORCID
- Yang, Xiuying
- Brobst, Daniel
- Chan, Wing Suen
- Tse, Margaret Chui Ling
- Herlea-Pana, Oana
- Ahuja, Palak
- Kwong, Zara Sau Wa
- Zhang, Ning
- Chow, Simon Kwoon Ho
- Cheung, Wing Hoi
- Louie, Jimmy Chun Yu
- Griffin, Timothy M.
- Nong, Wenyan
- Hui, Jerome Ho Lam
- Noh, Hye Lim
- Saengnipanthkul, Suchaorn
- Kim, Jason K.
- Lee, Chi Wai
- Chan, Chi Bun
- Venue
- Science Signaling
- Published
- 2019-08-13
- Volume
- 12
- Issue
- 594
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC7219567
- OpenAlex
- W2966949203
- Cited by
- 99
- References
- 69
- Citations by year
- 2026: 11 · 2025: 17 · 2024: 14 · 2023: 18 · 2022: 13 · 2021: 17 · 2020: 7 · 2019: 2
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (2U2C-DK093000)
- Presbyterian Health Foundation (Seed Grant Program)
- National Natural Science Foundation of China (81470159)
- CAMS Initiative for Innovative Medicine (CAMS-I2M 2016-I2M-3-007)
- Hong Kong government Research Grant Council (GRF17113817)
- HKU Research Committee Seed Funding Programme for Basic Research (201606159006)
- Drug Innovation Major Project (2018ZX09711001-003-005)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- brain-derived neurotrophic factor, myokines, skeletal muscle, metabolic flexibility, fuel selection, fasting, sexual dimorphism, muscle atrophy, autophagy, insulin resistance, metabolic myopathies, myofiber necrosis, energy homeostasis
- MeSH terms
- Animals, Female, Male, Muscle Proteins, Muscular Atrophy, Sex Characteristics, Signal Transduction, Mice, Knockout, Muscle, Skeletal, Brain-Derived Neurotrophic Factor, Mice
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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