When mice get obese from eating lots of fat, their brain's hunger neurons stop responding as strongly to fat in the stomach—even after they lose weight—but still respond normally to sugar or protein.
Scientific Claim
In mice fed a high-fat diet, diet-induced obesity is associated with a selective and long-lasting reduction in AgRP neuron inhibition in response to intragastric lipid infusion, but not to glucose or protein, suggesting a specific neural adaptation to dietary fat that persists after weight loss.
Original Statement
“Strikingly, AgRP neuron inhibition in response to lipid infusion was significantly decreased in DIO animals compared to their response at baseline... In contrast the response of AgRP neurons to glucose and protein was not altered in obese mice...”
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 title and abstract use causal language ('causes'), but the design is observational in mice with no randomization or control for diet vs. obesity per se. Only association can be inferred.
More Accurate Statement
“In mice, diet-induced obesity is associated with a selective and long-lasting reduction in AgRP neuron inhibition in response to intragastric lipid infusion, but not to glucose or protein, suggesting a specific neural adaptation to dietary fat that persists after weight loss.”
Evidence from Studies
Supporting (1)
Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat
When mice eat a lot of fat and get obese, their brain’s hunger neurons stop responding as strongly to fat in the stomach—even after they lose weight. But these neurons still respond normally to sugar or protein, meaning the brain gets 'used to' fat in a way that doesn’t go away.