When mice become obese, their brain’s hunger neurons don’t respond as strongly to ghrelin—the 'hunger hormone'—so they don’t eat as much even when given extra ghrelin, and this doesn’t fix itself after they lose weight.
Scientific Claim
In mice, diet-induced obesity is associated with partial resistance of AgRP neurons to ghrelin stimulation, which reduces ghrelin-induced feeding behavior and is not restored after weight loss, indicating a persistent disruption in hunger signaling.
Original Statement
“Following six weeks of HFD exposure, we observed a clear reduction in this ability of ghrelin to activate AgRP neurons... Subsequent weight loss did not restore the responsiveness of AgRP neurons in DIO mice to ghrelin...”
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 demonstrates association between obesity and ghrelin resistance, but cannot establish causation due to observational design and potential confounders like leptin elevation.
More Accurate Statement
“In mice, diet-induced obesity is associated with partial resistance of AgRP neurons to ghrelin stimulation, which reduces ghrelin-induced feeding behavior and is not restored after weight loss.”
Evidence from Studies
Supporting (1)
Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat
When mice get fat from eating high-fat food, their brain's hunger neurons stop responding well to the hunger hormone ghrelin—and even after they lose weight, those neurons still don’t respond properly, so they keep feeling less hungry than they should.