Whereas LHAVglut2 neurons from control mice maintained their responsivity to sucrose consumption, LHAVglut2 neurons from [the high fat diet] mice became progressively less responsive to sucrose consumption and less active at rest," the team writes in the study paper.
In other words, the neurons did not send such a strong "stop eating" signal to the brain when the mice consumed sugar or when the mice were resting. Instead, the animals overate and developed obesity.
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