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Skin inflammation may increase risk of developing type 2 diabetes

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Inflammatory skin disorders, such as psoriasis, may directly increase the risk of type 2 diabetes, according to a new study presented this week at a UK endocrinology conference.

The findings indicate that improving skin health could be of major importance for the control of blood sugar and lowering diabetes risk, according to researchers.

“The laboratory model we used in this study closely-resembles many of the major hallmarks of psoriasis”

Elizabeth Evans

Around 2-3% of the world’s population has the chronic inflammatory disorder psoriasis, where the immune system attacks skin cells, resulting in too much growth of younger ones and leading to itchy red sores.

The researchers noted that, unfortunately, there was currently no cure for psoriasis, with patients having to use treatments to alleviate the symptoms throughout their life.

To add to this burden, they highlighted that previous studies have suggested that having psoriasis increases the risk of developing type 2 diabetes.

However, the specific biological mechanisms linking the two disorders are unknown, they noted.

If defined, these mechanisms could lead to new therapies to treat patients suffering from skin problems and reduce the risk of type 2 diabetes, said the researchers.

In their 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 an attempt 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.

“We have observed some changes caused by the condition which reflect what is seen in a pre-diabetic patient”

Elizabeth Evans

Ms Evans said: “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.”

Next, Ms Evans and her colleagues said they planned to determine which skin derived factors were released during psoriasis, and the impact they have on the development of diabetes.

She said: “If we can pin point 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,” she added.

The study was presented this week as a poster – titled Skin-endocrine regulation of whole-body metabolism – at the Society for Endocrinology annual conference in Glasgow.

The society’s 2018 annual conference was held at the Scottish Event Campus between 19 and 21 November.

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