Insulin may play a key part in the development of obesity by acting directly on the brain's reward circuitry.
Jens Brüning at the Max Planck Institute for Neurological Research in Cologne, Germany, and his group genetically engineered mice in which they could inactivate insulin signalling in parts of the mid-brain that drive feelings of motivation and reward. The engineered mice ate more than control mice and became obese. Along the way, they developed mild insulin-resistant diabetes, although their metabolism was otherwise unaffected.
If similar mechanisms occur in obese humans, the authors say, it could help to explain why they tend to eat compulsively.
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Cellular cues to compulsive eating. Nature 474, 422 (2011). https://doi.org/10.1038/474422b
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DOI: https://doi.org/10.1038/474422b
