Helena Edlund

Biography

Professor Umeå Centrum för Molekylär Medicin (UCMM)

Research Interest

Typ2 diabetes is historically a disease that primarily affects older people but is also strongly associated with obesity. Obesity leads to elevated levels of free fatty acids that are deposited and converted into fats in different tissues. There is a clear link between obesity, fat deposits in different organs such as liver and development of insulin resistance. However, diabetes only develops when the insulin-producing beta cells cease to function and can no longer produce enough insulin to compensate for insulin resistance. More and more data also indicate that obesity in itself leads to decreased beta cell function. How, however, obesity, and thus increased concentrations of circulating free fatty acids in the affected individual, leads to impaired beta cell function is unknown. The causes of beta cell disability are due to a variety of molecular mechanisms, but characteristic of beta cells in developed type 2 diabetes is the presence of amyloid. In the insulin-producing beta cells, the amyloid of type2 is diabetic predominantly of a protein called Islamic Amyloid Polypetide, abbreviated IAPP. We mainly study molecular mechanisms behind amyloid formation and loss of beta cell function in the onset of diabetes. One of the cellular processes we study is autophagy and its role in preserving beta cell function. We mainly study molecular mechanisms behind amyloid formation and loss of beta cell function in the onset of diabetes. One of the cellular processes we study is autophagy and its role in preserving beta cell function. We mainly study molecular mechanisms behind amyloid formation and loss of beta cell function in the onset of diabetes. One of the cellular processes we study is autophagy and its role in preserving beta cell function.