IP6K1 Identified As Possible Key Protein Target in Treatment of Obesity and Type 2 Diabetes

In a series of studies led by Assistant Professor Anutosh Chakraborty of The Scripps Research Institute Florida campus, scientists have identified a key protein that promotes fat accumulation in animal models by slowing the breakdown and expenditure of fat and encouraging weight gain. It is no secret that losing weight is difficult. Each year brings a new popular diet, “guaranteed” to succeed, yet the explosion of obesity in the United States continues. Current anti-obesity medications are only partly effective, due to substantial side effects, the temporary nature of the weight loss, and the non-responsiveness of a considerable number of patients. The studies directed by Dr. Chakraborty were published in The International Journal of Biochemistry & Cell Biology (September 2016), Molecular Metabolism (August 21, 2016), and, most recently, The Journal of Clinical Investigation (October 4, 2016). Please see titles and links to each of these articles below. “We found that the protein IP6K1 (image) is a viable target in obesity and type 2 diabetes,” Dr. Chakraborty said. “We also discovered that an inhibitor of the protein known as TNP decelerates what is known as diet-induced obesity and insulin resistance.” In the last few years, enhancing energy expenditure has emerged as an attractive strategy to combat obesity and diabetes, although how this might be accomplished remains something of a mystery simply because the mechanisms by which the body maintains its energy balance is complex. The new studies point to IP6k1 (inositol hexakisphosphate kinase-1), specifically its inhibition, as a potentially rich target. Dr. Chakraborty and his colleagues found that deleting IP6K1 in fat cells enhanced energy expenditure and protected animal models from diet-induced obesity and insulin resistance.
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