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CaMKK2 Enzyme and Appetite Control

Researchers at Duke University Medical Center have reported that suppression of the CaMKK2 enzyme in mice resulted in lowered appetite, lower weight, and improved blood sugar management.

Activation of the CaMKK2 enzyme is one step in the pathway stimulated when the hormone ghrelin reaches the hypothalamus in the brain. CaMKK2 in turn activates AMPK, another enzyme, which is known to stimulate animals to eat.

The scientists first used a molecular inhibitor that blocked CaMKK2 receptors in mice. Those mice at significantly less food, and lost weight. So next the researchers studied a group of mice that do not make CaMKK2, and used the same inhibitor. It had no effect, suggesting that it was indeed the effect on CaMKK2 that was responsible for the appetite control.

What came as somewhat of a surprise were the results of the next study, in which both the normal mice and those lacking CaMKK2 were each divided into two groups -- one fed a low-fat diet, and the other group getting a high-fat diet. For normal mice, the high fat diet led to diabetes, while the low-fat diet did not. In the mice missing CaMKK2 however, both groups stayed healthy -- none developed diabetes.

Dr. Tony Means who led the research said:

Remarkably, we find that blocking CaMKK2 in the brain prevents the deposits of fat in liver and skeletal muscle that are characteristic of obese, diabetic patients.

Further research is on-going to determine how this effect is achieved, and to see if CaMKK2 has any beneficial effects which could lead to detrimental consequences if that enzyme is blocked.