correlational
Analysis v1
13
Pro
0
Against

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)

13

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.

Contradicting (0)

0
No contradicting evidence found