Early research suggests that inhibiting glucose transport in the skin may be a safe, effective therapy for psoriasis.
A research team led by Dr. Richard Wang, assistant professor of dermatology at the University of Texas Southwestern in Dallas, noting that glucose was of greater importance to rapidly-proliferating cells, inactivated the glucose transporter protein GLUT1 in a mouse model of psoriasis—both genetically and through the use of inhibiting medications. This reduced disease-associated skin overgrowth and inflammation in the mice.
“This study provides a window for the treatment of various diseases by specifically targeting the metabolic requirements of hyperproliferative skin diseases. It also broadens our understanding of changes in skin metabolism in response to physiological stressors,” Dr. Wang said in a press release from the university on May 4, 2018.
Importantly, these treatments did not compromise the skin’s development or functionality.
Dr. Wang's team were able to decrease inflammation with topical application of a GLUT1 inhibitor. That inhibitor also had a notable effect on psoriatic human skin grown in a dish, suppressing both inflammation and the expression of disease-associated genes.
The findings were published in Nature Medicine (April 16, 2018; 24:617-627).
“Although I would still consider our findings preliminary, they have the potential to provide novel therapeutic approaches for inflammatory and neoplastic skin diseases,” Dr. Wang said.