Obese mice don’t get as excited (in brain terms) when they see food—but when they lose weight, this brain response comes back, unlike their response to fat or hormones.
Scientific Claim
In mice, diet-induced obesity is associated with a reversible blunting of AgRP neuron inhibition in response to sensory food cues (e.g., sight/smell of food), which normalizes after weight loss, unlike responses to gut-derived signals.
Original Statement
“Diet-induced obesity reversibly attenuates the AgRP neuron inhibition in response to food presentation... Subsequent weight loss restores the responsiveness of AgRP neurons to exterosensory cues...”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study shows association between obesity and reversible sensory blunting, but causal language ('attenuates', 'restores') overstates the evidence. Design cannot prove causation.
More Accurate Statement
“In mice, diet-induced obesity is associated with a reversible blunting of AgRP neuron inhibition in response to sensory food cues, which normalizes after weight loss, unlike responses to gut-derived signals.”
Evidence from Studies
Supporting (1)
Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat
When mice get fat from eating fatty food, their brain stops reacting as strongly to the sight or smell of food — but when they lose weight, that reaction comes back. However, their brain still doesn’t respond well to signals from the gut, even after losing weight.