Mechanism of hyperphagia contributing to obesity in brain-derived neurotrophic factor knockout mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model study (Oxford Level 5).
PubMed 23069761 · doi:10.1016/j.neuroscience.2012.09.078
What was done
Researchers investigated the feeding mechanisms of obesity in a brain-derived neurotrophic factor (BDNF) knockout mouse model that spared sufficient brainstem BDNF to avoid perinatal lethality. They conducted meal pattern and microstructure analyses to evaluate satiation and satiety. They also measured meal-induced c-Fos activation in the nucleus of the solitary tract and the dorsal motor nucleus of the vagus nerve (DMV), and assessed vagal sensory neuron counts.
What was found
The abstract reports no numeric values. Qualitatively, BDNF knockout mice exhibited deficits in satiation and satiety resulting in increased meal size and increased meal frequency. Meal-induced c-Fos activation was unchanged in the nucleus of the solitary tract but was increased in the DMV. Vagal sensory neuron numbers were also reported as altered in BDNF knockout mice.
Why it matters
The findings indicate that BDNF deficiency induces hyperphagia via impaired satiation and satiety, possibly mediated by altered vago-vagal reflexes rather than direct deficits in vagal afferent signaling to the solitary tract.
Limits
This is an animal study using a genetically modified mouse model, limiting direct translation to human physiology. The abstract provides no sample sizes, numerical data, variance estimates, or specific descriptions of the directional changes in vagal sensory neuron numbers.
Cited by
- supports Genetically reducing BDNF levels by approximately 50% causes mice to overeat and develop obesity.