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T2DM

How the body responds to T2DM drug treatment

New model allows researchers to study the long-term physiological effects of the development and treatment of T2DM
Dr Bilal Omar

Researchers at Lund University in Sweden have developed a new mouse model which they claim answers some of the questions of what actually happens in the body when type 2 diabetes develops and how the body responds to drug treatment.

"The animal models for type 2 diabetes studies that have previously existed have not been optimal because they use young mice. Our idea was to create a model that resembles the situation in the development of type 2 diabetes in humans,” said Dr Bilal Omar, one of the authors of the study. "The goal is to design drugs and treatments which, if they can't cure the disease, can at least give the patient a better quality of life for several years."

Reporting their research in the journal Diabetologia, the study authors explain that the new middle-aged mouse model enabled them to study long-term physiological effects of the development and treatment of type 2 diabetes in a completely new way.

Long-term studies of the middle-aged mouse model will be better than previous studies at confirming how drugs for type 2 diabetes function in humans, they state.

Previous studies have shown that dipeptidyl peptidase-4 (DPP4) inhibitors stimulate insulin secretion and increase beta cell mass in rodents. However, in these models hyperglycaemia has been induced early on in life and the treatment periods have been short.

Therefore, they decided to explore the long-term effects of DPP4 inhibition on insulin secretion and beta cell mass.

The researchers fed normal mice fatty food over a long period from the age of eight months (middle age), until the end of their natural lives at the age of two years. The mice become overweight, and develop high blood sugar levels and reduced insulin release, as expected before the onset of type 2 diabetes.

"Throughout the period we were able to study the process that leads to the development of type 2 diabetes with a lifestyle like that of people predisposed to the condition," said Omar.

They were able to confirm that fatty foods lead to inflammation in the islets of Langerhans in the pancreas, which produce insulin.

"Another aspect of our findings is that the inflammation in the islets was caused by a high-fat diet,” said Professor Bo Ahrén, co-author of the study.

“Even if it is too early to draw parallels with the diet of humans, it makes it doubtful whether a high-fat diet over a long period should be recommended, as in the low carb, high fat diet.”

After one month of a high fat diet, the mice were given the DPP4 inhibitor vildagliptin for a further 11 months.

The results showed that beta cell function and glucose tolerance were significantly improved by vildagliptin with both diets however, beta cell area was not significantly different between vildagliptin-treated mice and controls.

"What was so interesting and exciting was that the mice that were treated with dipeptidyl peptidase-4 (DPP4), a class of drugs used for type 2 diabetes, did not develop inflammation and they maintained good insulin production,” he added. “They were still obese, but had normal blood sugar, were otherwise healthy and lived longer."

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