Obese mice don't respond as well to a gut hormone (CCK) that normally tells the brain to stop eating fat—and even after they lose weight, this blunted response doesn't come back.
Scientific Claim
In mice with diet-induced obesity, the inhibition of AgRP neurons by the gut hormone cholecystokinin (CCK) is significantly reduced and remains impaired after weight loss, which may underlie the persistent blunting of fat-induced satiety signals.
Original Statement
“Both the neuronal and behavioral responses to CCK were reduced following six weeks of HFD exposure... Returning DIO mice to a chow diet for four weeks failed to rescue this CCK resistance...”
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 reduced CCK response, but cannot prove causation due to lack of randomization and confounding variables (e.g., hyperleptinemia). Causal language is inappropriate.
More Accurate Statement
“In mice, diet-induced obesity is associated with a reduced inhibition of AgRP neurons by the gut hormone cholecystokinin (CCK), and this impairment persists 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 fatty food, their brain’s hunger neurons stop responding properly to a fullness signal from the gut (CCK), and even after they lose weight, this signal still doesn’t work right — making it harder to feel full.