New research has investigated ways of preventing the “hunger hormone” ghrelin from driving people who have lost weight into a rebound. An enzyme with a metabolic function was found to reduce ghrelin’s influence, which may point to a new way of managing weight gain.

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Scientists are looking into the possibility of using one enzyme to halt the overproduction of ghrelin, which “tells” us when to feel hungry.

According to data from the Centers for Disease Control and Prevention (CDC), 36.5 percent of adults and around 17 percent of children and adolescents in the United States live with obesity.

The main approach to obesity management and prevention is adopting a more healthful lifestyle, including a more balanced diet and more physical exercise.

However, studies have shown that many individuals who shed weight after dieting have a tendency to rebound and regain the extra kilos that they worked so hard to eliminate.

This, researchers explain, is due to a rise in ghrelin levels. Ghrelin is the so-called hunger hormone, which tells our bodies when to feel hungry and when they have had enough to eat. This increase is due to our bodies’ adaptive response to the often drastic dietary changes that lead to weight loss.

Now, researchers from the Mayo Clinic – which is based in Rochester, MN – are aiming to develop a new approach to prevent weight regain in the aftermath of a diet. Dr. Stephen Brimijoin and his colleagues tested the effects of an enzyme with the potential of blocking or limiting ghrelin production on mice.

The researchers reported their findings in the Proceedings of the National Academy of Sciences.

Dr. Brimijoin and his team used mice in a context simulating the situation of people who have shed excess weight through dieting, but who are then are liable to regain it due to the increase in ghrelin levels.

The scientists wondered whether or not using butyrylcholinesterase might help to regulate the overproduction of ghrelin after weight loss.

Butyrylcholinesterase is an enzyme naturally produced in the liver that plays a role in eliminating certain poisonous substances from the system, as well as metabolizing certain quantities of drugs such as cocaine.

The encoded enzyme was inserted into a neutralized virus, which was then administered to the mice with the aim of targeting ghrelin production.

It was found that boosting butyrylcholinesterase levels both correlated with a significant drop in the levels of the hunger hormone and moderated its activity. As a result, the animals adopted more balanced eating habits and did not gain any extra weight.

This happened after only one exposure to the enzyme-boosting procedure and had long-term outcomes, allowing the mice to avoid weight gain for the rest of their lives.

Dr. Brimijoin and his colleagues hope that these findings might lead not only to a more effective approach to obesity management, but also to preventive treatments for other metabolic diseases.

These include diabetes, metabolic syndrome (characterized by a combination of risk factors that could lead to coronary heart disease and other cardiovascular problems), and fatty liver disease (characterized by excess fat accumulating in the liver).

The scientists are pleased with the success of their research so far, but they emphasize the need to replicate these results in human participants before confirming the effectiveness of this approach.

We think this approach – combined reduction of calories and hormone – may be a highly successful strategy for long-term weight control. Given the growing obesity crisis worldwide, we are working hard to validate our findings for medical intervention.”

Dr. Stephen Brimijoin