When food was digested by the mice, they found, the gut released hormones into the blood stream, not just within the intestines, and up into the brain, where the hormone receptors were triggered. Mice with GCC knew when to stop, but hormone receptor-deficient mice never got the message that their stomachs were full. They simply kept eating and became obese.
"They got to be diabetic and developed the metabolic syndrome, fatty livers, etc." Dr. Waldman said. "We ruled out usual suspects: gastroenterology function was normal. They weren't more sedentary than wild type mice. And they did not have abnormal metabolism. We realized they just have a different appetite."
The research offers up a new neural-gut axis that explains appetite more, but it still begs some questions: Do obese people possess little to no GCC? And if so, does that mean obese people have a genetic disposition to gain weight?
It's possible, said Dr. Waldman, but it's still unclear. There is the possibility that obese people do not have the receptor or they do not release enough hormones to trigger the receptor. More studies are needed to better explain this, he added.
"Obesity could be biological, and not behavioral," said Dr. Waldman. "But there is no evidence here that confirms that; however, knowing this new information opens that possibility."
|Contact: Steve Graff|
Thomas Jefferson University