Psoriasis is a common inflammatory skin condition, affecting an estimated 2.2 percent of people in the United States.
For decades, we have known that psoriasis increases the risk of developing type 2 diabetes. However, the exact nature of this connection is unclear.
Recently, researchers from King’s College London in the United Kingdom designed a series of experiments to gain insight into the link.
Lead author Elizabeth Evans presented their findings at a recent annual conference of the Society for Endocrinology, in Glasgow, U.K.
Psoriasis is the most common autoimmune disease in the U.S.
Currently, medicines can address symptoms, but because there is no cure, treatment tends to continue throughout an individual’s life.
In people with psoriasis, skin cells are replaced too quickly.
Usually, it takes 3–4 weeks to develop cells in the deeper layers of skin. As they mature, they slowly rise to the surface.
However, psoriasis causes immature skin cells to reach the surface in less than 1 week, after which they die and flake off. This leads to red, itchy patches of skin.
The team from King’s College studied human and animal skin samples, looking for any molecular alterations associated with psoriasis that might induce diabetes.
They used an experimental model of psoriasis created by applying imiquimod — an immune response modifier — to mouse and human skin.
Psoriasis, inflammation, and insulin
The researchers found that skin from mice with psoriasis demonstrated inflammation and insulin resistance, a risk factor for diabetes.
This resistance means that cells are not responding correctly to the hormone insulin and are not removing glucose from the bloodstream.
Fat tissue, in particular, took up glucose less easily, and the researchers measured a reduction in levels of glucose transporter type 4, a receptor necessary for moving glucose into fat cells.
Also, beta cells in the mice with psoriasis produced more insulin than those in the unaffected mice. The researchers believe that this overproduction is an attempt to compensate for insulin resistance.
“The laboratory model we used in this study closely resembles many of the major hallmarks of psoriasis, and we have observed some changes caused by the condition which reflect what is seen in a prediabetic patient.”
In short, the inflammation associated with psoriasis caused insulin resistance and increased insulin production. The triggers for both these effects were produced by the skin.
This is just the start of their research. The team wants to identify the factors released by the psoriatic skin that may play a role in developing diabetes.
The results of this investigation will improve our understanding of the common skin disease, and they may also help us gain insight into diabetes.
Evans says, “If we can pinpoint novel skin-derived factors that are directly affecting blood sugar control, they may lead to potential therapeutic targets for the treatment of diabetes or insulin resistance.”
Eventually, this research may help reduce the risk that people with psoriasis will develop diabetes. As Evans explains, “Finding out if skin-derived factors which alter blood sugar control are lower when treatment for psoriasis is properly adhered to would be very interesting, as it may lower a patient’s risk of developing type 2 diabetes.”
While these early results mark the beginning of a long road ahead, there is enormous potential to improve psoriasis treatment, reduce diabetes risk in people with psoriasis, and gain insight into how diabetes works.
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