5th Annual VCU 3MT® Competition, held on October 18-19, 2019.
https://scholarscompass.vcu.edu/threemt/10Transcription:
I see quite a few women in the audience, well I have some good news for
you. It’s great to be a woman, you have a lower risk of developing autism,
addiction, Schizophrenia, and now adding to this list liver damage. Non-Alcoholic
Fatty Liver Disease (NAFLD) is the most common liver disorder with an estimated
economic impact of $292 billion in United States alone. Fibrosis is the first
stage of liver damage and hence can be targeted for therapeutics. Interestingly
pre-menopausal women are protected from fibrosis but the exact cause for this
is not known. Our lab specializes in studying lipids which are the compounds
used for energy storage, signaling, and they also form structures of our
cellular membranes. A lipid in which we are particularly interested is named
Sphingosine 1 phosphate or S1P, it has been known to be a critical regulator of
many important physiological functions including cancer, diabetes, and
fibrosis. It also has a reputation of being the bad guy or a villain as it
promotes fibrosis in multiple organs, therefore our lab created a mouse model
in which liver cells were unable to produce this lipid. The reasoning behind
this was simple that by removing this villain we can get rid of fibrosis and
that is exactly what we saw in male mice which were protected from high fat
diet induced fibrosis, but to our surprise female mice which are usually protected
had severe liver damage. It is something that has not been seen before. Upon
further investigation we observed that a female sex hormone known as estrogen promotes
S1P which in turn protects livers from damage. This study reveals two important
things 1) The notorious bad guy named S1P has in fact been the knight and
shining armor for women all along. 2) One organ’s villain is another organ’s
hero, S1P which has been shown to cause fibrosis in other organs has an
opposite role in liver. Therefore, by keeping these two points in mind we can
now use this knowledge to develop therapies specifically targeted towards liver
damage and we can finally balance out this tipping scale.
