Gene Removal May Prevent Obesity


Inhibiting theIPK61 protein was observed to stop weight gain in animals.

Removing a gene that encodes for a certain protein was seen to prevent animals from developing obesity and diabetes in a new study published by Molecular Metabolism.

Many scientists have been studying the complicated mechanisms involved with weight loss due to the growing proportion of individuals with obesity. While it is understood that exercise burns calories, researchers are now looking at how the body burns calories to stay warm during cold weather.

In previous studies, the researchers discovered that the IP6K1 protein promotes fat accumulation in animal models by slowing fat breakdown. In the new study, deleting the gene for IP6K1 protected against weight gain and diabetes.

The investigators found that the effect was seen regardless of diet, even at thermoneutral temperatures (approximately 86⁰F). This finding suggests that blocking IP6K1 can help burn energy regardless of outside climate, according to the study.

“In genetically altered animal models that lack IP6K1, we found that deletion dramatically protects these knock-out mice from diet-induced obesity and insulin resistance regardless of the temperature in the environment,” said lead researcher Anutosh Chakraborty, PhD. “When we inhibited the enzyme with chemical compounds, the results were similar.”

Accounting for temperature is important for obesity research since animals in lower temperatures will lose more weight trying to maintain body temperature, compared with those in higher temperatures, according to the study.

Since humans can use heaters, wear warm clothing, and take other measures to increase body temperature, targeting pathways that reduce body weight, regardless of temperature, could be significant for human obesity research.

Findings from the new study suggest that creating an IP6K1 inhibitor could elicit energy burning comparable to that seen in low temperatures.

“If we delete IP6K1, the animals gain less body weight because they simply expend more energy—regardless of temperature,” Dr Chakraborty said. “That’s important because blocking weight gain by enhancing energy expenditure in a thermoneutral environment is harder and thus, targeting IP6K1 is expected to be successful in ameliorating obesity in humans.”

Regardless of diet, the animal models were seen to lose weight. If translated to humans, diet would no longer be an important part of weight loss for those taking an IPK61 inhibitor.

However, a poor diet can result in numerous other health problems, including cardiovascular disease and other chronic diseases.

More research is needed to determine if an IP6K1 inhibitor would be successful in humans.

“If you’re developing an anti-obesity drug based on inhibiting IP6K1, our new findings show that there are potentially very few restrictions for its use—a subject would lose weight even on a high-fat diet, and nobody would have to sit in a refrigerator to make it work,” Dr Chakraborty concluded.

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