Even in overweight mice, the brain’s TRPM2 sensor still works — it can still turn on heat production in fat tissue.
Scientific Claim
TRPM2 expression in POMC neurons is not affected by high-fat diet feeding, as ADPR still depolarizes POMC neurons and increases body temperature in obese mice, suggesting preserved TRPM2-mediated thermogenic capacity in diet-induced obesity.
Original Statement
“Similar to the findings in NCD-fed mice, ADPR treatment induced POMC neuron depolarization in the ARC in HFD-fed mice (9 of 12 neurons). ... i.c.v. injection of ADPR significantly increased both BAT and core body temperature in HFD-fed mice.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
The study directly compared responses in normal and high-fat diet mice and found no loss of TRPM2 function. The claim accurately reports preserved activity without inferring causality or human applicability.
Evidence from Studies
Supporting (1)
The potential role of hypothalamic POMCTRPM2 in interscapular BAT thermogenesis
Even in mice that ate a high-fat diet and became obese, their brain cells still responded to a chemical that turns on heat production, meaning the system that helps burn fat for heat still works fine.