Psoriasis increases risk for type 2 diabetes, finds study

A new study finds that people with inflammatory skin disorders, such as psoriasis, might be at increased risk of type 2 diabetes.

Findings of the study, presented at the Society for Endocrinology annual conference in Glasgow, indicate that improving skin health could be of major importance for the control of blood sugar and lowering diabetes risk.

Psoriasis is a chronic inflammatory disorder where the immune system attacks skin cells, resulting in too much growth of younger skin cells leading to itchy red sores, affects about 2-3% of the global population. Currently, there is no cure for with patients having to use treatments to alleviate the symptoms throughout their life.

Previous studies have shown that having psoriasis increases your risk of developing type-2 diabetes, adding to the burden. However, the specific biological mechanisms linking the two disorders are unknown, and if defined, they could lead to new therapies to treat patients suffering from skin problems and reduce the risk of type-2 diabetes.

Elizabeth Evans and colleagues at King's College London used animal and human skin models, to look for changes caused by psoriasis which may influence the development of diabetes.

Key Findings:

• Mice with psoriasis showed changes indicative of insulin resistance, a key feature of diabetes development where insulin fails to stimulate glucose uptake in cells. Changes included a decrease in glucose uptake capacity in a fat tissue under the skin and increased insulin production from insulin-producing cells, indicating that the body is trying to compensate for the lack of glucose uptake.


• Similar alterations were seen in fat and islet cells outside the body when exposed to the culture liquid used to support inflamed skin samples, suggesting that inflamed skin releases chemical signals to cause the changes.

In this study, Elizabeth Evans and colleagues at King's College London used animal and human skin models, to look for changes caused by psoriasis which may influence the development of diabetes. Mice with psoriasis showed changes indicative of insulin resistance, a key feature of diabetes development where insulin fails to stimulate glucose uptake in cells. Changes included a decrease in glucose uptake capacity in fat tissue under the skin and increased insulin production from insulin-producing cells, indicating that the body is trying to compensate for the lack of glucose uptake. Similar alterations were seen in fat and islet cells outside the body when exposed to the culture liquid used to support inflamed skin samples, suggesting that inflamed skin releases chemical signals to cause the changes.

"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 pre-diabetic patient," commented Elizabeth Evans.

Next Elizabeth and her colleagues plan to determine which skin-derived factors are released during psoriasis, and the impact they have on the development of diabetes.

Elizabeth Evans said, "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. Additionally, 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."