New mechanism of lipid droplet growth
Researchers from Tsinghua University and the University of New South Wales in Australia have recently revealed a new mechanism for the formation of lipid droplets. The related paper "Perilipin1 promotes unilocular lipid droplet formation through the activation of Fsp27 in adipocytes" was published on March 12 Nature-Communication (Nature Communications) magazine. Leading this research is Peng Li, a professor at the School of Life Sciences at Tsinghua University and a researcher at the Tsinghua-Peking University Life Science Joint Center. He is currently deputy dean of the School of Life Sciences of Tsinghua University and chief scientist of the 973 Protein Project. It is mainly engaged in the study of molecular apoptosis mechanisms and metabolic diseases such as obesity, diabetes, and atherosclerosis. He has published more than 20 influential articles in top international magazines such as Cell, Nature, Nature cell biology, etc. Among them, research papers on cell death published in Cell have been cited nearly 3000 times, and have been selected as the most influential in this field One of the strong papers. Disturbance of lipid metabolism can cause various metabolic diseases such as obesity, diabetes, fatty liver, atherosclerosis, etc., which seriously endanger human health. Lipid Droplet, as the core organelle of lipid metabolism, can specifically store neutral lipids, and its number and size are closely related to the balance of lipid metabolism. However, until now scientists have known very little about the mechanism of lipid droplet growth and formation. Adipocyte-specific lipid droplet-related protein Fsp27 is a protein that plays an important role in the process of energy metabolism and obesity. Recent reports have shown that it binds to the surface of lipid droplets, and can co-localize with the lipid droplet binding protein Perilipin, and at the same time has the effect of promoting the accumulation of triglycerides in cells. It is not expressed in preadipocytes, but is abundantly expressed when adipocytes are differentiated; it is expressed in brown and white adipose tissues, but it is hardly expressed in other tissues. The latest research confirms that Fsp27 has the functions of promoting energy reserve, inhibiting lipolysis, leading the formation of single-room large lipid droplets, and participating in the balance and regulation of whole-body energy. Inhibition or knockout of Fsp27 leads to the formation of a large number of small lipid droplets, increased lipolysis, and decreased fat deposition. These studies suggest that by affecting the expression of Fsp27, the accumulation of lipid droplets in adipocytes can be changed. It may be a molecular switch that controls the shape and number of lipid droplets, thus becoming a potential target for treating obesity and related metabolic diseases. However, the molecular mechanism by which Fsp27 regulates the formation of lipid droplets is not yet clear. In this article, the researchers found that Perilipin1 (Plin1) is an activator of Fsp27. Plin1 interacts with the CIDE-N domain of Fsp27, which significantly promotes Fsp27-mediated lipid exchange, lipid transfer, and lipid droplet growth. The functional synergy of Plin1 and Fsp27 is a necessary condition for efficient lipid droplet growth in adipocytes. Depletion of any protein can damage lipid droplet growth. In addition, the researchers found that the CIDE-N domain of Fsp27 formed a homodimer, and disrupting CIDE-N homodimerization could prevent Fsp27-mediated lipid exchange and transfer. Interestingly, the researchers found that Plin1 can restore the activity of Fsp27 CIDE-N homodimerization-deficient mutants. The new study reveals a new mechanism for lipid droplet growth and single-cell lipid droplet formation, confirming that Fsp27 and Plin1 synergistically promote the formation of lipid droplets in adipocytes by initiating enhanced lipid transfer events.
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