The fatter you get, the more you can eat or because your brain 'brakes' fail.

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energy imbalance is the main cause of obesity, and we often find in our lives that obese people seem to eat more. Professor Garrett Stuber of the Department of Psychiatry at the University of Southern California and his co-scientists published a study on obesity in the June 28 issue of Science: Obesity can affect the excitation of nerve cells in the brains of mice, suppressing the "brake" function of the nerves that control eating.
the outer area of the hemthovascular brain is the key area to regulate physiological behavior such as animal diet and energy balance. The researchers isolated cells in the outer part of the lower pasum brain in mice on a normal diet and 18th in a high-fat diet, and detected changes in gene expression in individual cells. They found that the region specifically expressed vesicle glutamate transporter 2 (Vglut2) glutamate energy neuron LHAVglut2 gene expression changes the most. The neuron is highly correlated with the body's body mass index (BMI) at the genetic level.
, the researchers tested the effects of sucrose feeding stimulation on the excitation of LHAVglut2 neurons in the brains of normal mice. The results showed that the lower the appetite of mice, the higher the excitement of LHAVglut2 neurons, while the detection of the response of obese mice to sucrose stimulation found that the level of excitement of LHAVglut2 neurons decreased. That is to say, the excitation of LHAVglut2 neurons in the outer region of the heteroc brain may be a "brake" signal for animals to eat, and normally the neurons have high levels of excitement when the animals eat, and are sensitive to "brakes", which inhibits large intakes of food. Obese people inhibit the activity of LHAVglut2 neurons, which affects the function of the "brake".
Professor Stephen Bogland of the Hodgkiss Brain Institute at the University of Calgary in Canada, in a commentary published in the journal Science at the same time, said the study offers a promising hypothesis that diet-induced obesity undermines the ability of LHAVglut2 neurons to "slow down" their eating. "Subsequent studies should also consider the role of other nerve cell substations in the LHA region in regulating eating."