Blocking A Single Protein Could Cure Obesity
Dr.Tony Means, PhD, and Duke University researchers halted the activity of a brain enzyme, CaMKK2, in mice which caused them to lose weight by decreasing their appetite.
They have located an target in the brain which could potentially function as an appetite suppressant, weight loss promoter and help to control blood sugar.
Scientists have sought to understand appetite for food and and suppression of the neural pathways that stimulate appetite. Research is to find ways for obese and overweight people to better limit their weight and lower their chances of developing diabetes, heart disease and other related medical.
The enzyme CaMKK2 is a promoter of the appetite pathways in the hypothalamus portion of the brain. The empty stomach releases a hormone called ghrelin. Ghrelin causes a series of signals that cause in increase in appetite for food.
Dr. Means and his team think that CaMKK2 in the ghrelin pathway is a likely answer to obesity. Ghrelin activates AMPK, a protein that makes animals eat and become fat. Researchers tested their theory in several ways.
The CaMKK2 protein (an enzyme) was blocked in mice using an enzyme inhibitor and then they observed food intake. The CaMKK2 blocked mice ate markedly less food than the normal mice during the test. The CaMKK2 blocked mice also lost a significant amount of weight.
The next group of mice were a group that do not make the CaMKK2 protein and observed that the molecule inhibitor did not change feeding behavior or reduce weight. “The fact that blocking CaMKK2 worked in normal mice to make them eat less and lose weight, but not in mice missing the enzyme, provides compelling evidence that CaMKK2 signaling is a requirement for appetite control,” Means said.
In mice without the CaMKK2 enzyme (both the ones born without CaMKK2 and the blocked CaMKK2 group), the researchers noticed that the mice stayed healthy regardless of what kind of diet they consumed. The CAMKK2-negative mice apparently were protected from changes that lead to diabetes in a high-fat diet.
Blocking CaMKK2 in the brain prevents the accumulation of fat in liver and skeletal muscle that are seen in obese, diabetic patients, The team hopes to understand the mechanism responsible for this beneficial effect, and tofind more potent drugs that can inhibit CaMKK2.
ref: http://dukemednews.org/news/article.php?id=10315
