14 DAY TRIAL // It is well known that our body weight is the result of genetics, food intake and energy waste.
Keeping a healthy weight is the result of a balance, in which also hormones like those produced by the thyroid are involved.
A new investigation from Rockefeller University points that brain cell receptors activated by sex hormones possess an important role in balancing the body weight. The metabolic syndrome, a group of symptoms like obesity, insulin resistance and decreased physical activity, was inflicted in female mice when brain zones sensitive to estrogen were turned off. "It is well documented that mice missing the gene for estrogen receptor become obese," says Pfaff, head of the Laboratory of Neurobiology and Behavior. "But because every cell in these 'knockout' mice has been missing estrogen signaling from birth, these results are confounded by potential effects on overall brain development. Using a targeted approach, we interfered with the receptor's synthesis only in the neurons in the ventromedial nucleus of the hypothalamus, and found that these mice also become obese."
The ventromedial nucleus, an area rich in estrogen receptors, was already proven by previous researches as having a main role in maintaining the energy balance: its impairment turns mice obese.
The team employed a novel genetic engineering technique to assess the role of the estrogen receptor in the ventromedial nucleus; the researchers employed a virus to insert strands of DNA stretch in the neurons of the nucleus that stops the synthesis of the estrogen receptor. The engineered mice immediately started to gain weight, even if the food quantity they ingested remained the same. "We found that the increase in food was secondary, the weight gain occurred first and the mice started to eat more simply to maintain their new body weight," says Musatov.
"Estrogen signaling obviously plays an important role in the ventromedial nucleus to help maintain normal body weight."
These mice were also less active and their metabolism was lower, developing the same symptoms like in human obesity: glucose intolerance and resistance to insulin.