Type 1 @entity6 is caused by an immune-mediated destruction of the insulin-secreting beta cells in the pancreas. The disease can become clinically apparent at any age. At diagnosis, there is invariably some residual beta cell function and more so in adults than in @entity1 . Recent studies--including one conducted mainly in Belgium--have provided proof of principle that short-term anti-T-cell antibody treatment is able to preserve residual beta cell function for at least 18 months. The resultant stabilizing effect on metabolic control is expected to delay or limit chronic complications in these @entity1 . With a similar goal in mind, nonuremic C-peptide negative @entity1 are offered beta cell transplantation. The outcome of these implants looks promising but their final applicability hinges on finding ways to induce immune tolerance to the donor beta cells. A widespread application, however, will only occur if the shortage of viable @entity1 donor cells can be overcome. Both xenotransplantation and stem cell therapy provide possible strategies to solve this problem and represent areas of intense investigation. The ultimate goal is prevention of clinical disease. Studies by the Belgian @entity6 Registry and others in first degree family members of type 1 @entity6 @entity1 have refined the identification of individuals at very high risk of hyperglycaemia so that new immunological treatments can be tested in the prediabetic phase.

New therapies aimed at the preservation or restoration of beta cell function in type 1 XXXX .

@entity1 :: ('9606', 'Species') :: ['children', 'human', 'patients'] @entity6 :: ('MESH:D003920', 'Disease') :: ['Diabetes', 'diabetic', 'diabetes']
@entity6 :: (MESH:D003920,Disease) :: ['diabetes']
