Research from the Dartmouth-Hitchcock Norris Cotton Cancer Centre, have discovered a potential new drug that prevents obesity in mice.
The researchers discovered that a receptor, that is present in almost all cells, plays an important role in the body’s metabolism. The research showed that by blocking the receptor with the use of a drug, the mice on a high-fat diet did not become any fatter than the mice on a low-fat, controlled diet. Obese mice were also tested in the study and with the use of the drug they were able to drop the weight. Throughout the testing, no ill side effects were observed.
The obesity pandemic is estimated to cost the global economy £27bn a year. Obesity is a contributor to several cancers including breast, colon and pancreatic. Stopping the obesity epidemic could be a critical aid in preventing and treating numerous cancers.
The receptor found in most cells is known as AHR, it’s known to primarily combat exposure to environmental chemicals, also plays a large role in the body’s metabolism. By blocking the AHR receptor it not only prevented but reversed obesity in the mice. The findings of the study are newly published in the International Journal of Obesity.
Craig Tomlinson PhD, Senior Research Scientist, said: We carried out experiments showing that when a drug named NF, known to block the AHR, mice did not become any fatter than mice on a low-fat control diet. In these experiments, we allowed the mice to become obese on a high-fat diet, and then half the mice were switched to the high-fat diet containing the AHR blocker NF.
“Over the next few weeks, the mice switched to the high-fat diet containing NF dropped to the same bodyweight as those mice on the low-fat diet. The remaining mice on the high-fat diet became obese. Again, no ill effects were observed.”
Mechanisms behind the receptor
Tomlinson’s team also investigated the processes behind how the AHR, when blocked by NF, prevented and reversed obesity. Using known already known knowledge of the receptor, the researchers discovered that in the liver cells and in fat cells, the receptor – when blocked by the drug – failed to produce several key genes that are required for fat storage and synthesis.
They concluded that they were able to prevent and reverse obesity by blocking the activity of the AHR, which is due to key genes which are using regulated by the receptor are involved in fat metabolism.
Tomlinson, explained: “Few to no studies have shown that obesity can be reversed by a drug treatment; it is even rarer to know the underlying cellular mechanism.”
The researchers are continuing to investigate several key questions including, those around the dietary compounds in the food we eat that activate the AHR to cause obesity, and the role that gut bacteria play regarding the AHR and obesity.
However, most importantly, the team have commenced clinical trials to determine whether the AHR may serve as a target to reduce obesity in humans.