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Weight Gain Linked to Brain Enzyme E-mail
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Researchers at Albert Einstein College of Medicine of Yeshiva University have found obese_womanthat overactivity of a brain enzyme may play a role in preventing weight gain and obesity . The findings were reported in Cell Metabolism.

To understand what drives hunger and causes metabolic disease, many scientists have focused on the hypothalamus, an almond-sized structure located deep within the brain that controls body temperature, hunger, and thirst. Specialized nerve cells in the hypothalamus sense whether the body contains adequate amounts of nutrients and stored body fat. The cells then send out signals telling other parts of the brain to adjust food intake, metabolic rates, and physical activity accordingly -keeping the body's caloric intake in balance with calories burned.

To learn more about these nutrient-sensing pathways and how they go awry in metabolic disorders, researchers at Einstein focused on an enzyme called p70 S6 Kinase 1, or S6K, which plays a role in regulating the growth and proliferation of all cells, including nerve cells.

"It turns out that this enzyme, and the pathway it regulates, is nutrient sensitive - that is, S6K activity increases in the presence of carbohydrates and protein," says the study's principal investigator, Gary J. Schwartz, Ph.D., professor of medicine and neuroscience at Einstein. "This led us to believe that S6K might not only be involved in maintaining the structure and function of individual cells, but also in regulating the energy balance of the whole body."

To test this hypothesis, the researchers injected rats with special viruses that selectively raise or lower S6K activity. The viruses were injected directly into the lower-middle, or mediobasal, portion of the hypothalamus, an area rich in nutrient-sensing nerve cells.

"When we raised the activity of the enzyme, we saw reductions in food intake, in body weight, and in production of peptides [small chains of amino acids] that normally stimulate feeding," says Dr. Schwartz. "When we lowered S6K activity, we saw essentially the opposite response."

The way increased S6K activity reduced the rats' food intake is important, says Dr. Schwartz: reducing the average size of meals rather than changing the number of meals over the course of a day. So the animals apparently were sated faster and therefore ate less at every meal.

In another experiment, the researchers tested whether increased S6K activity would protect against the natural tendency of mammals on a high-fat diet to overeat. People deal with all those calories by putting on extra weight and becoming insensitive to insulin - two of the hallmarks of metabolic syndrome, a group of risk factors that raise the risk of heart disease and type 2 diabetes.

When animals on a high-fat diet were given the S6K-enhancing virus, they overate less and gained weight more slowly than control animals, the researchers report. In addition, the virus-enhanced animals had lower body-fat levels and better glucose tolerance than the control group.

Overall, the study shows that S6K acts as a kind of food-sensing thermostat in mammals, increasing or decreasing feeding behavior and metabolism to maintain a normal energy balance. "These findings show that it may be possible to control obesity and other human metabolic disorders by developing drugs that regulate S6K activity," says Dr. Schwartz.

Clémence Blouet, Ph.D., a postdoctoral fellow at Einstein, is the lead author of the paper. The other co-author is Hiraku Ono, Ph.D., also a postdoctoral fellow at Einstein.

About Obesity

Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, exceeds healthy limits. It is commonly defined as a body mass index (BMI) (weight divided by height squared) of 30 kg/m2 or higher. Although obesity is an individual clinical condition, some authorities view it as a serious and growing public health problem.

A large number of medical conditions have been associated with obesity. Health consequences are categorized as being the result of either increased fat mass (osteoarthritis, obstructive sleep apnea, social stigma) or increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease). Mortality is increased in obesity, with a BMI of over 32 being associated with a doubled risk of death. There are alterations in the body's response to insulin (insulin resistance), a proinflammatory state and an increased tendency to thrombosis (prothrombotic state).

Disease associations may be dependent or independent of the distribution of adipose tissue. Central obesity (male-type or waist-predominant obesity, characterized by a high waist-hip ratio), is an important risk factor for the metabolic syndrome, the clustering of a number of diseases and risk factors that heavily predispose for cardiovascular disease. These are diabetes mellitus, Type 2 diabetes, high blood pressure, high blood cholesterol, and triglyceride levels (combined hyperlipidemia).

Apart from the metabolic syndrome, obesity is also correlated with a variety of other complications. For some of these complaints, it has not been clearly established to what extent they are caused directly by obesity itself, or have some other cause (such as limited exercise) that causes obesity as well. Health complications may include from this condition may include:
 
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