Scientists have identified a protein that acts as a kind of traffic controller for fat inside cells, revealing a mechanism that could help explain how the body regulates energy storage and why things go wrong in metabolic disease. The discovery provides a new avenue for treating obesity and type 2 diabetes
Researchers from The University of New South Wales (UNSW) have found that the protein CHP1 is essential for both producing fat molecules and directing them to where they need to go. But first, we need to understand a bit more about how our cells store fat.
Inside cells, fat is tucked away in lipid droplets, which act like tiny storage units that house reserve energy but also play a key role in building and repairing cell membranes. To fill the droplets, cells use a production line known as the glycerol-3-phosphate (G-3-P) pathway. This line makes two important products: triacylglycerols, the main form of stored fat, and glycerophospholipids, which form the scaffolding of cell membranes.
The first step on this line is the most critical, and it’s carried out by enzymes known as microsomal GPATs. Two of these – GPAT3 and GPAT4 – do most of the work in fat-making tissues. Scientists knew these enzymes were key players in cellular function, but until now it wasn’t clear how they were switched on or guided to the right place in the cell.
The UNSW team discovered that CHP1 is the protein that regulates this. It acts as both a stabilizer and an activator of GPAT3 and GPAT4, ensuring they fill their natural roles. But just as importantly, CHP1 also helps guide them to lipid droplets, so they can actually channel new fat molecules into storage. Without CHP1, lipid droplets became significantly smaller, because the machinery that fills them is no longer in place.
Essentially, removing CHP1 led to a dramatic reduction in the size of the lipid droplets, suggesting that this protein is a key regulator of fat metabolism within a cell.
“Our findings provide a clearer picture of the intricate machinery that controls how cells store fat,” said lead author Guang Yang from UNSW’s School of Biotechnology and Biomolecular Science. “Understanding this process is a critical step towards developing new strategies to address a range of metabolic disorders like obesity and diabetes.”
While it’s a long way from these findings to treatment, by uncovering how CHP1 drives the activation and direction of these key enzymes gives researchers a promising new target in combatting metabolic disorders.
The study also highlights that lipid droplets – once thought to be inert fat stores – are in fact active organelles that manage how fat is stored and used in cells. Dysfunctional lipid storage underlies a wide range of health conditions, with obesity and diabetes just two of them.
The study was published in the journal Proceedings of the National Academy of Sciences.
Source: The University of New South Wales via Scimex
