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The lighter side of BDNF
Open accessAbstract
Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that “faulty” circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity.
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“BDNF is known to affect the regulation of feeding and energy metabolism [218–221].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [218]
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Additional file 2 of Brain-derived neurotrophic factor associated with kidney function
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Additional file 5 of Brain-derived neurotrophic factor associated with kidney function
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Additional file 4 of Brain-derived neurotrophic factor associated with kidney function
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Metadata
- Authors
- Noble, E. E., Billington, C. J., Kotz, C. M., & Wang, C.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Wang, ChuanFeng
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2011-05
- Volume
- 300
- Issue
- 5
- Pages
- R1053-R1069
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC3293512
- OpenAlex
- W2096180958
- Cited by
- 284
- References
- 292
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 15 · 2023: 19 · 2022: 13 · 2021: 13 · 2020: 23 · 2019: 15 · 2018: 15 · 2017: 15 · 2016: 25 · 2015: 25 · 2014: 23 · 2013: 28 · 2012: 28
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK050456, R01DK080782)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- brain-derived neurotrophic factor, TrkB receptor, hypothalamus, hippocampus, energy homeostasis, feeding behavior, energy expenditure, neurogenesis, neuroplasticity, obesity, eating disorders, neurotrophins
- MeSH terms
- Animals, Feeding and Eating Disorders, Brain, Eating, Energy Metabolism, Feeding Behavior, Homeostasis, Humans, Neuronal Plasticity, Obesity, Signal Transduction, Brain-Derived Neurotrophic Factor, Receptor, trkB, Neurogenesis
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