The speakers discussed state-of-the-art data and models regarding the brain as an initiator of obesity and as a target organ of peripheral feedback signals that regulate feeding behaviour. Reports of the talks by Barry Levin, Mary Dallman, and Gregory Morton are published in the September 1 issue of The Journal of Physiology, and they provide intriguing insights into the physiological basis of obesity.

As examples, Dr. Levin suggested that the physiological processes which drive all of us to seek and ingest food and limit energy expenditure during periods of negative energy balance provide an irresistible drive to regain lost adipose stores in weight-reduced obese individuals. This provides a potential basis for the well-recognized difficulty of maintaining weight loss. Dr. Dallman reported that conditions of reduced food allowance and chronic stress excite central neural networks that may lead toward abdominal obesity. This provides a potential link between stress and obesity.

Finally, Dr. Morton discussed that during a reduction in energy stores or circulating nutrients, the brain initiates responses to restore and maintain energy and glucose homeostasis. In contrast, in times of nutrient abundance and excess energy storage, the brain promotes reduced food intake and increased energy expenditure. An impaired ability of the brain to respond to hormonal or nutrient-related signals would be predicted to favour weight gain and insulin resistance and may contribute to the development of obesity and type 2 diabetes.

Together, these exciting presentations suggested potentially useful avenues of future research, which will hopefully provide improved preventive and therapeutic insights.

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