Impaired intestinal afferent nerve satiety signalling and vagal afferent excitability in diet induced obesity in the mouse

DM Daly, SJ Park, WC Valinsky… - The Journal of …, 2011 - Wiley Online Library
DM Daly, SJ Park, WC Valinsky, MJ Beyak
The Journal of physiology, 2011Wiley Online Library
Non‐technical summary Obesity is known to result from energy intake in excess of
expenditure. What is not known is how individuals are able to eat in excess of their energy
needs. We show that after chronic consumption of a high fat diet (which causes obesity),
intestinal sensory nerves are less responsive to chemicals released from the gut during a
meal (cholecystokinin and 5‐hydroxytryptamine) as well as to distension of the gut as might
occur during a meal. This appears to be due to the fact that the ability of the nerve cells to be …
Non‐technical summary  Obesity is known to result from energy intake in excess of expenditure. What is not known is how individuals are able to eat in excess of their energy needs. We show that after chronic consumption of a high fat diet (which causes obesity), intestinal sensory nerves are less responsive to chemicals released from the gut during a meal (cholecystokinin and 5‐hydroxytryptamine) as well as to distension of the gut as might occur during a meal. This appears to be due to the fact that the ability of the nerve cells to be excited is impaired. This suggests that consumption of an unhealthy diet that leads to obesity causes decreased signalling from the intestine, which may lead to increased food intake and contribute to further weight gain, or allow the maintenance of excess weight and obesity.
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