ArticleNeuroscience2013
Mechanism of hyperphagia contributing to obesity in brain-derived neurotrophic factor knockout mice.
Article in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Association between Obesity and Circulating Brain-Derived Neurotrophic Factor (BDNF) Levels: Systematic Review of Literature and Meta-Analysis.International journal of molecular sciences · 2018Pooled it
- TrkB Receptor Antagonism Enhances Insulin Secretion and Increases Pancreatic Islet Size in Rats Fed a Cafeteria-Style Diet.Biomedicines · 2025Article
- Identification and functional validation of rare coding variants in genes linked to monogenic obesity.Obesity (Silver Spring, Md.) · 2024Article
- Exercise-induced appetite suppression: An update on potential mechanisms.Physiological reports · 2024Review
- BDNF haploinsufficiency induces behavioral endophenotypes of schizophrenia in male mice that are rescued by enriched environment.Translational psychiatry · 2021Article
- Heterozygous rare genetic variants in non-syndromic early-onset obesity.International journal of obesity (2005) · 2020Article
- Maternal Obesity Alters Neurotrophin-Associated MAPK Signaling in the Hypothalamus of Male Mouse Offspring.Frontiers in neuroscience · 2019Article
- Exercise, Obesity and CNS Control of Metabolic Homeostasis: A Review.Frontiers in physiology · 2018Review
- NaMolecular metabolism · 2017Review
- Effect of food deprivation or short-term Western diet feeding on BDNF protein expression in the hypothalamic arcuate, paraventricular, and ventromedial nuclei.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.Journal of the American Heart Association · 2015Article
- A murine toolbox for imaging the neurovascular unit.Microcirculation (New York, N.Y. : 1994) · 2015Review
- Reduced intestinal brain-derived neurotrophic factor increases vagal sensory innervation of the intestine and enhances satiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Loss of neurotrophin-3 from smooth muscle disrupts vagal gastrointestinal afferent signaling and satiation.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Vagal afferent controls of feeding: a possible role for gastrointestinal BDNF.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2013Review
- Molecular and neural bases underlying roles of BDNF in the control of body weight.Frontiers in neuroscience · 2013Article
- Early postnatal overnutrition: potential roles of gastrointestinal vagal afferents and brain-derived neurotrophic factor.Physiology & behavior · 2012Review
- Development of the vagal innervation of the gut: steering the wandering nerve.Neurogastroenterology and motility · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Global-heterozygous and brain-specific homozygous knockouts (KOs) of brain-derived neurotrophic factor (BDNF) cause late- and early-onset obesity, respectively, both involving hyperphagia. Little is known about the mechanism underlying this hyperphagia or whether BDNF loss from peripheral tissues could contribute to overeating. Since global-homozygous BDNF-KO is perinatal lethal, a BDNF-KO that spared sufficient brainstem BDNF to support normal health was utilized to begin to address these issues. Meal pattern and microstructure analyses suggested overeating of BDNF-KO mice was mediated by deficits in both satiation and satiety that resulted in increased meal size and frequency and implicated a reduction of vagal signaling from the gut to the brain. Meal-induced c-Fos activation in the nucleus of the solitary tract, a more direct measure of vagal afferent signaling, however, was not decreased in BDNF-KO mice, and thus was not consistent with a vagal afferent role. Interestingly though, meal-induced c-Fos activation was increased in the dorsal motor nucleus of the vagus nerve (DMV) of BDNF-KO mice. This could imply that augmentation of vago-vagal digestive reflexes occurred (e.g., accommodation), which would support increased meal size and possibly increased meal number by reducing the increase in intragastric pressure produced by a given amount of ingesta. Additionally, vagal sensory neuron number in BDNF-KO mice was altered in a manner consistent with the increased meal-induced activation of the DMV. These results suggest reduced BDNF causes satiety and satiation deficits that support hyperphagia, possibly involving augmentation of vago-vagal reflexes mediated by central pathways or vagal afferents regulated by BDNF levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.