IIT Bombay researchers develop peptide that reduces fat release from liver cells

A team of scientists at the Indian Institute of Technology (IIT) Bombay, in collaboration with researchers from IISER Pune and IISER Kolkata, has developed a small peptide that reduces the secretion of fats into the bloodstream. The peptide, named KTDP, was shown to lower the release of cholesterol and triglycerides by nearly 50 percent in laboratory-grown liver cells and in zebrafish.

The findings were published in the journal Proceedings of the National Academy of Sciences (PNAS). While the results are promising, the peptide has not yet been tested in humans, and further research is needed to evaluate its safety and effectiveness.

Fats such as cholesterol and triglycerides are essential for the body but can become harmful when present in excess in the blood. High levels of low-density lipoprotein (LDL) cholesterol and triglycerides are major risk factors for heart attacks and other cardiovascular diseases.

Current treatments, such as statins, are effective at lowering cholesterol by reducing its production in the liver or increasing its clearance from the blood. However, options for reducing triglycerides remain limited.

The IIT Bombay team took a different approach. Instead of targeting how fats are produced or broken down, they aimed to prevent fats from being released from the liver into the bloodstream.

Inside liver cells, fats are stored in small compartments called lipid droplets. These droplets are transported to specific locations within the cell by a motor protein called kinesin-1. At those locations, the fats are repackaged into very low-density lipoproteins (VLDL) and exported into the blood.

The peptide KTDP is derived from kinesin-1. When introduced into cells, it disrupts the transport of lipid droplets, preventing them from reaching the site where they are packaged for export. As a result, less fat is secreted into the bloodstream.

Professor Roop Mallik of IIT Bombay explained that the peptide essentially blocks the fat from being carried to the right location. Without that delivery, the fat cannot be repackaged and released.

An important finding was that blocking fat export did not cause dangerous fat buildup inside the liver. Instead, the fats were redirected to mitochondria, the cell's energy-producing structures, where they were broken down to generate energy.

The researchers caution that the work is at an early stage. The peptide has only been tested in cell cultures and zebrafish, and human trials are needed to confirm its potential as a treatment.

Despite these limitations, the study opens a new strategy for managing high blood lipids. By reducing the liver's export of fats, it may complement existing therapies and offer a novel way to lower cardiovascular risk.