While the hunger hormone exists on its own in the body, it does not cause us to feel hungry unless acted upon by a specific enzyme. This enzyme, ghrelin O-acyl transferase (GOAT, for short), acylates the hormone, thereby causing the person to feel hungry. Until this study, it was assumed that GOAT enzymes were associated with fatty acids produced by the body while fasting, largely because the hunger hormone levels spike during fasting and before meals, which is when people feel the most hunger.
However, what the scientists found was that the levels of the activator fatty acid, GOAT, actually coincided with ingested dietary fats, rather than fatty acids produced by the body. In other words, what we eat can make us hungrier than what we don't.
In addition, a previously published study, done by scientists in Geneva, has linked ghrelin levels to storage of fats in the body. The study showed that ghrelin levels were linked not only to promoting the intake of food, but also in the processing of adipose (fatty) foods by the body. By introducing higher levels of ghrelin into the brains of rats, they observed that the rats stored more energy as fats. The authors had recommended further research into ghrelin and its purposes within the body, in order to stem the tide of the worldwide obesity epidemic.
This study, then, is a perfect follow-up, since it shows how ghrelin is activated within the body. "When exposed to certain fatty foods, mice with more GOAT gain more fat," said UC associate professor of psychiatry and internal medicine Matthias Tschöp. "Mice without GOAT gain less fat since their brain does not receive the 'fats are here, store them' signal."
"Our GOAT studies in mice offer an explanation of what could have been happening during the longer fasting periods in these human studies," he said. "Without dietary fats, ghrelin peaks remain inactive and don't affect storage of fat."
The study is expected to revolutionize obesity treatments, such as gastric bypass surgery. Gastric bypass has been a popular way to treat obesity, not only because of the drastic reduction in actual stomach size inherent to the surgery, but also because of the sharp drop in appetite and spike in metabolism that occurs directly thereafter. According to Tschöp, the drop in appetite could be due to the bypassing of the gut region in which reside the GOAT/ghrelin pairing, which causes the ghrelin peaks to be unactivated. In other words, the gastric bypass bypasses the hunger mechanism.
"Hunger Hormone Activated By Fats In The Food We Eat"
"A Matter Of Fat"
http://www.medicalnewstoday.com/articles/44910.php
www.medicalnewstoday.com
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- Scientists found that what we eat can make us hungrier than what we don't.
- By introducing higher levels of ghrelin into the brains of rats, the rats stored more fat.
- The study is expected to revolutionize obesity treatments, such as gastric bypass surgery.




