In obese mice, turning on hunger neurons just before eating doesn’t make them eat much more—but turning them on while they’re eating does. This suggests their brain’s feeding system becomes less sensitive to normal hunger signals.
Scientific Claim
In mice, diet-induced obesity is associated with a reduced ability of AgRP neuron stimulation to drive feeding via pre-stimulation (natural timing) compared to concurrent stimulation (forced activation), suggesting downstream circuitry may become less sensitive to physiological levels of AgRP activity.
Original Statement
“In obese mice, we found that concurrent stimulation induced a bigger effect on food intake than pre-stimulation... whereas in lean animals the effect of these two stimulation protocols was indistinguishable...”
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 differential stimulation effects, but cannot prove causation. The interpretation of 'reduced sensitivity' is plausible but inferred.
More Accurate Statement
“In mice, diet-induced obesity is associated with a reduced ability of AgRP neuron stimulation to drive feeding via pre-stimulation compared to concurrent stimulation, suggesting downstream circuitry may become less sensitive to physiological levels of AgRP activity.”
Evidence from Studies
Supporting (1)
Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat
When mice get obese from eating fatty food, their hunger neurons stop responding as well to natural hunger signals—like stomach cues—making them less likely to eat even when they should. This suggests their brain’s hunger system gets 'numb' to normal signals.