NCT00336674

Trial of Intranasal Insulin in Children and Young Adults at Risk of Type 1 Diabetes

A Randomised, Double-blind, Placebo-controlled Trial of Intranasal Insulin (440 IU) in Children and Young Adults at Risk of Type 1 Diabetes: Intranasal Insulin Trial II

• Status: Completed
• Phase: Phase 2
• Study type: Interventional
• Enrollment: 110 (actual)
• Sponsor: Melbourne Health · Academic / Other
• Sex: All
• Age: 4 Years – 30 Years
• Healthy volunteers: Not accepted

Summary

In people with type 1 diabetes the beta cells of the pancreas no longer make insulin because the body's immune system has attacked and destroyed the beta cells. It is thought that exposure of the mucous membranes to insulin may cause act like a vaccine effect whereby protective immune cells are stimulated and these then counteract the "bad" immune cells that damage the beta cells. This study aims to determine if intranasal insulin can protect beta cells and stop progression to diabetes in individuals who are at risk.

Detailed description

Autoimmune diseases are the outcome of dysregulated immune responses to self-antigens. Type 1 diabetes (T1D), previously known as insulin-dependent or juvenile diabetes, is an autoimmune disease in which the body's immune system reacts against and destroys the insulin-producing β cells in the islets of the pancreas. T1D classically affects children and young adults. Approximately 15% of people with diabetes have this form of the disease and no treatment is currently available to prevent it. Asymptomatic individuals in the pre-clinical stage of T1D can be identified by the presence of circulating antibodies to the islet autoantigens (pro)insulin, glutamic acid decarboxylase (GAD) and tyrosine phosphatase-like insulinoma antigen 2 (IA2). (Pro)insulin is the only autoantigen that is specific for β cells and several lines of evidence demonstrate that it plays a key role in driving autoimmune β-cell destruction. The ability to use self-antigens as tools to induce protective immunity, free from the side effects of conventional non-specific immunosuppression, is the 'Holy Grail' of autoimmune disease therapy. Animal models provide proof-of-concept for such antigen-specific therapy. For example, in the non-obese diabetic (NOD) mouse, a model of spontaneous T1D, transgenic over-expression of proinsulin in antigen-presenting cells in the immune system during development or in transferred bone marrow stem cells completely prevented diabetes. On a more practical and translatable level, immune tolerance to an antigen can be achieved by administering antigen to the mucosal immune system. Thus, immune responses to antigen are suppressed by feeding antigen ('oral tolerance') or by administering antigen to the naso-respiratory mucosa .

Conditions

• Type 1 Diabetes

Interventions

Type	Name	Description
BIOLOGICAL	Intranasal insulin	440IU Insulin
OTHER	Placebo	Placebo insulin carrier solution containing benzalkonium chloride and glycerol

Timeline

• Start date: 2006-12-01
• Primary completion: 2019-11-13
• Completion: 2019-11-13
• First posted: 2006-06-14
• Last updated: 2020-10-08

Locations

6 sites across 2 countries: Australia, New Zealand