Even when obese mice don’t feel hungry, turning on their hunger neurons with light makes them eat normally again—meaning the problem is the brain isn’t turning on the hunger signal, not that the body can’t respond to it.

Scientific Claim

In mice with diet-induced obesity, optogenetic stimulation of AgRP neurons can restore normal food intake during fasting, suggesting that the neurons themselves are underactivated rather than downstream circuits being unresponsive.

Original Statement

“Optogenetic stimulation of AgRP neurons could rescue this decreased feeding in DIO mice... This suggests AgRP neurons are not fully activated by fasting in DIO animals, and that optogenetic stimulation supplies this missing activation.”

From study:Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat

Evidence Quality Assessment

Claim Status

overstated

Study Design Support

Design supports claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

While optogenetics provides strong evidence for underactivation, the study is still observational in nature and cannot prove causation in humans. 'Suggests' is appropriate; 'proves' or 'causes' are not.

More Accurate Statement

“In mice with diet-induced obesity, optogenetic stimulation of AgRP neurons is associated with restored food intake during fasting, suggesting that the neurons are underactivated rather than downstream circuits being unresponsive.”

Evidence from Studies

Supporting (0)

No supporting evidence found

Contradicting (1)

Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat

Cohort Study

Animal

2020 Jul 28

The study found that in obese mice, the brain’s hunger neurons stop responding properly to food signals, even after losing weight — so it’s not that they’re just sleepy and need a wake-up call, they’re broken in a deeper way.

Source Study

Obesity causes selective and long-lasting desensitization of AgRP neurons to dietary fat

Score: 13

DOI: 10.7554/eLife.55909

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