Researchers at the UT Southwestern Medical Center in the United States have discovered that a new role for Perilipin 5, which is usually located on the surface of lipid droplets in cells, acts as a regulator of fat metabolism in the nucleus.
In obese people and rodent, excess fat accumulates in tissues that are not specifically used to store fat, such as skeletal muscle, heart, and liver. Researchers say this accumulation can lead to dysfunction in these tissues.
Decomposing large amounts of fat can overload the body's metabolic system, flooding small cell mitochondria, they turn fat into fuel for work or heat. The researchers said: "If you use fuel to make the plant too loaded, then it will not work well. Then, these cells only have a portion of the processed fat, which may be toxic to the mitochondria and cause type 2 diabetes. Insulin resistance that occurs in the body."
Endurance athletes - like obese insulin resistance patients, they accumulate the same amount of fat in their muscle cells abnormally. Some studies have found that they have higher levels of Perilipin 5, and this new discovery by the UTSW research team may explain Why such athletes can use the increase in fat storage to increase the motivation of exercise while avoiding the toxicity of increased muscle fat.
In cell culture and mouse experiments, the UTSW team found that when cells are stimulated to release fat stored in fat droplets, Perilipin 5 can leave the surface of the droplets and move to the nucleus of the cell where it is another protein, PGC-1α, works together to promote more and more efficient mitochondrial production. In this way, Perilipin 5 helps to match the mitochondria's ability to burn fat with intracellular fat load.
These findings may eventually lead to new therapies for obesity-related diabetes, perhaps a new drug that mimics one aspect of Perilipin 5 or its function.
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