Control of hyperphagia prevents obesity in BDNF heterozygous mice.
Level 5 - mechanism / opinion, no new human data
Non-human animal research (Level 5 by CEBM rules).
PubMed 15570174 · doi:10.1097/00001756-200412030-00022
What was done
Brain-derived neurotrophic factor (BDNF) heterozygous mice with reduced BDNF levels were maintained on a pair-feeding regimen over a prolonged period, receiving the amount of food normally consumed by control mice, to determine whether hyperphagia or metabolic dysfunction drives obesity in this model.
What was found
The abstract reports no numerical values or statistical metrics. BDNF-deficient mice restricted to normal control intake did not develop obesity and maintained normal blood glucose levels.
Why it matters
It demonstrates that hyperphagia, rather than primary metabolic or energy expenditure defects, is the primary driver of obesity and hyperglycemia resulting from BDNF deficiency in mice.
Limits
The study was conducted in a mouse model, limiting direct translatability to human energy homeostasis. The abstract does not report sample sizes, specific feeding durations, body weight measurements, glucose concentrations, or variance metrics.
Cited by
- supports Genetically reducing BDNF levels by approximately 50% causes mice to overeat and develop obesity.