A multimedia mosaic of moments at GIST
The possibility of curing metabolic disorders such as obesity, fatty liver and diabetes opens up. - The activation of AMPK, the energy sensor of human cells, curbs the increase of blood sugar and body fat. - AMPK-controlling gene & protein, CRBN, is discovered. - Finding by Professor Chul-Seung Park’s research team was published in the journal of the American Diabetes Association in February. □ When short on energy, human cells curb energy consumption and control metabolism. A breakdown in such a mechanism leads to the development of metabolic diseases such as obesity and diabetes. The AMPK protein is called the energy sensor of cells, which is activated in cells short on energy and its artificial activation opens up the possibility of treating metabolic diseases such as obesity, fatty liver and #2-type diabetes. ○ A group of researchers led by professor Chul-Seung Park, School of Life Science at Gwangju Institute of Science and Technology (GIST, President Young-Joon Kim) found that the cereblon protein (CRBN) directly combines with AMPK to suppress its function and proved the possibility that metabolic disorders such as obesity and fatty liver can be prevented or cured by suppressing CRBN, which will then activate AMPK. * AMPK(AMP-activated kinase): an enzyme which plays a key role in metabolism control and is reported to show low activity under metabolic diseases such as obesity and diabetes. AMPK is called the energy sensor of cells since it recognizes AMP, which increases when energy is in short, and thus curbs the consumption of ATP while activating its production. *Cereblon: a protein which is made from by a gene of the same name. Its function in human body is not known yet other than that it combines with thalidomide, a drug found to cause birth defects. There are also reports that the mutation of the cereblon gene causes minor mental retardation.