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Obesity and Neurons - Obesity treatment by manipulating neural pathways
A new study has shown that the reason some people can eat apparently what they want, get no exercise and still not gain weight, might be neurological. The study shows that people with a high-fat diet and low amounts of exercise who still somehow remain slim, might have a slightly different neurological circuitry then people with a high tendency towards gaining weight.

The study, led by the Australian Monash University, showed that a high-fat diet in some people can cause a group of cells in the brain to become insulated, effectively preventing and dampening the bodies signals. These signal, the hormone leptin among them, are responsible for telling the brain that the body is full and ready to burn energy. When the signal is dampened or completely absent, the brain has no way of telling when the body’s energy reserves have been replenished, and is in a state of constant appetite.

Professor Cowly, of the Monash University stated that there are two clear results from this findings.

“We discovered that a high-fat diet caused brain cells to become insulated from the body, rendering the cells unable to detect signals of fullness to stop eating," Professor Cowley said. "Secondly, the insulation also created a further complication in that the body was unable to detect signals to increase energy use and burn off calories/kilojoules."
The research has shown that a group of supporting brain cells, the tanycytes, becomes insulated with fat as a result of a high-fat diet, thus preventing an important system in the brain, the melanocortin system, from receiving signals from the body and connecting with other neural circuitry. The melanocortin system determines the level of appetite and body’s energy expenditure levels.

According to Cowly, this research presents a critical link in obesity research, and can provide with new approaches to treating obesity and weight related problems.

"These neuronal circuits regulate eating behaviors and energy expenditure and are a naturally occurring process in the brain. The circuits begin to form early in life so that people may have a tendency towards obesity even before they eat their first meal," Professor Cowley said.

Additionally, when the cells are insulated with fat and start dampening or preventing signals from the body, it becomes increasingly difficult for the person to start losing weight, as the body tries to prevent any unnecessary loss of energy.

A subsequent study, done in the UK, lead by researcher Dr Mohammad Hajihosseini, may provide a glimmer of hope for chronically obese people. After a study done in East Anglia, it has become increasingly clear that the fat insulation of tanycytes, although under genetic and prenatal influence, can be altered and significantly contributed to by environmental factors. This study showed that tanycytes can, in most cases, be altered throughout childhood and well into adulthood.

"This study has shown that the neural circuitry that controls appetite is not fixed in number and could possibly be manipulated numerically to tackle eating disorders," Hajihosseini said.

Unfortunately, they say it would be another 10-15 years before they can be ready to design and test a therapy aimed at obese human patients.

"The next step is to define the group of genes and cellular processes that regulate the behavior and activity of tanycytes," he said. "This information will further our understanding of brain stem cells and could be exploited to develop drugs that can modulate the number or functioning of appetite-regulating neurons."

The study is published in the Journal of Neuroscience.
T. L. Horvath, B. Sarman, C. Garcia-Caceres, P. J. Enriori, P. Sotonyi, M. Shanabrough, E. Borok, J. Argente, J. A. Chowen, D. Perez-Tilve, P. T. Pfluger, H. S. Bronneke, B. E. Levin, S. Diano, M. A. Cowley, M. H. Tschop. Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. Proceedings of the National Academy of Sciences, 2010; 107 (33): 14875 DOI:10.1073/pnas.1004282107
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