NCT00837759

Novel Therapy to Preserve Beta Cell Function in New Onset Type 1 Diabetes

Novel Therapy Combining Regenerative Stimuli Immunomodulation to Preserve Beta Cell Function in New Onset Type 1 Diabetes

• Status: Terminated
• Phase: Phase 2
• Study type: Interventional
• Enrollment: 7 (actual)
• Sponsor: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) · NIH
• Sex: All
• Age: 16 Years – 30 Years
• Healthy volunteers: Not accepted

Summary

Background: * Type 1 diabetes (T1D) occurs when the immune system attacks insulin-producing cells (beta cells) in the pancreas, resulting in their death. * Insulin injections currently are the best method for controlling blood sugar in individuals with T1D. However, animal studies have shown that the drugs sitagliptin and lansoprazole can help reverse beta cell damage or develop new beta cells. In addition, Diamyd has been shown to weaken the immune process that attacks pancreatic beta cells. Objectives: * To find out whether a combination treatment of sitagliptin, lansoprazole, and Diamyd will help maintain functioning beta cells and/or cause new beta cells to form. * To determine how the drug combination affects insulin doses and blood sugar control. * To determine whether the drug combination affects the immune response involved in T1D.

Detailed description

Type 1 diabetes (T1D) is the end result of immune mediated beta-cell destruction. It is generally accepted that at the time of T1D is diagnosed, an individual has lost most (60-80%) of his/her beta cell function. The loss of insulin-producing beta cells is believed to occur over a period of months to years and individuals can retain some endogenous insulin production even years after clinical diagnosis of diabetes. The presence of residual beta cell mass may signify a complex interplay between the auto-destructive immune response and the capacity for limited beta cell regeneration. When initiated at T1D onset, immunosuppression has been shown to preserve beta cell function, but with significant and limiting toxicities. Selectively targeting the pathogenic T-cells involved in T1D development and progression could achieve the same objective with less toxicity. Various studies of the non-obese diabetic (NOD) mouse model of spontaneous autoimmune diabetes have demonstrated that administering glutamic acid decarboxylase (GAD65), a beta cell autoantigen, can prevent the immune destruction and delay or prevent diabetes onset. Preclinical studies have also identified several growth factors, including epidermal growth factor (EGF), glucagon-like peptide 1 (GLP-1), and gastrin, that appear to promote beta cell proliferation. We seek to test the potential for preserving beta cell function early in the disease course of T1D by combining antigen-specific immunomodulation with regenerative stimuli.

Conditions

• Diabetes Mellitus Type 1
• Autoimmune Diabetes

Interventions

Type	Name	Description
DRUG	Insulin
DRUG	Lansoprazole
DRUG	Sitagliptin
BIOLOGICAL	Diamyd
DRUG	GAD65 (Diamyd)

Timeline

• Start date: 2009-02-01
• Primary completion: 2011-03-01
• Completion: 2011-03-01
• First posted: 2009-02-05
• Last updated: 2013-01-03
• Results posted: 2012-10-24

Locations

1 site across 1 country: United States