Scientists have identified a key protein that could be used as a treatment target for obesity and type 2 diabetes.
The discovery, made during a series of studies led by Assistant Professor Anutosh Chakraborty of The Scripps Research Institute in Florida, has raised hopes that by eliminating the IP6k1 protein (inositol hexakisphosphate kinase-1) fats will be broken down more easily, helping weight loss and cutting the risk of obesity and type 2 diabetes.
The researchers observed that the IP6K1 protein promotes fat accumulation in animals by slowing the breakdown and expenditure of fat and encouraging weight gain.
“We found that the protein IP6K1 is a viable target in obesity and type 2 diabetes,” said Chakraborty. “We also discovered that an inhibitor of the protein known as TNP decelerates what is known as diet-induced obesity and insulin resistance.”
Deleting IP6k1 in the fat cells of animal models was found to enhance energy expenditure and protect them from diet-induced obesity and insulin resistance.
The expenditure of fat energy is preceded by a process called lipolysis which breaks down stored fat into free fatty acids and glycerol to be used as energy in cells. When IP6K1 was deleted, it was found to affect interaction with another regulating protein and enhanced the breakdown of fats.
To assses how the IP6KI pathway could yield future weight loss treatments, the team analysed the impact of an IP6K inhibitor known as TNP [N2-(m-Trifluorobenzyl), N6-(p-nitrobenzyl) purine] on diet-induced obesity in animal models. TNP was found to significantly slow the onset of diet-induced obesity and insulin resistance.
“In addition, the compound facilitates weight loss and improves metabolic parameters when used in animals that are already obese,” said Chakraborty.
The studies were published in The International Journal of Biochemistry and Cell Biology, Molecular Metabolism and, most recently, The Journal of Clinical Investigation

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