New drug target may help prevent, reverse obesity

New drug target may help prevent, reverse obesity

Researchers have found a critical target in mice, which can prevent and reverse weight gain without side effects.

Washington, January 15

Researchers have found a critical target in mice, which can prevent and reverse weight gain without side effects, an advance which may lead to novel therapies to combat obesity.

According to the study, published in the International Journal of Obesity, a receptor found in almost all cells called AHR, known to combat exposures to environmental chemicals, plays a major role in the body’s metabolism.

“We carried out experiments showing that when a drug named NF and known to block the AHR, was added to a high-fat diet, mice did not become any fatter than mice on a low-fat control diet,” said Craig Tomlinson, study co-author from the Dartmouth-Hitchcock’s Norris Cotton Cancer Center in the US.

“Mice on the high-fat diet with no NF became very obese within the same time span. No ill effects were observed from the drug,” Tomlinson said.

In the study, the scientists allowed the mice to become obese on a high-fat diet, and then switched half of the rodents to a high-fat diet containing the AHR blocker NF.

Over the following weeks, the mice which were switched to the diet containing NF dropped to the same body weight as those on the low-fat diet.

“The remaining mice on the high-fat diet became obese. Again, no ill effects were observed,” Tomlinson said.

According to the scientists, the AHR regulates key genes involved in fat metabolism.

The current study revealed that in liver and fat cells, the AHR, when blocked by NF, fails to induce several key genes required for fat storage and synthesis.

Based on this finding, the researchers concluded that the prevention and reversal of obesity from blocking the activity of the AHR is due to key genes regulated by the AHR which are involved in fat metabolism.

“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,” Tomlinson said. —PTI

 

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