Interleukin-35 by Bettini at St. Judes

Title: Prevention of Autoimmune Diabetes by Ectopic Pancreatic β-Cell Expression of Interleukin-35

Quotes from Abstract:

Interleukin (IL)-35 is a newly identified inhibitory cytokine used by T regulatory cells to control T cell–driven immune responses. ...

Nonobese diabetic RIP-IL35 transgenic mice exhibited decreased islet infiltration with substantial reductions in the number of CD4+ and CD8+ T cells, and frequency of glucose-6-phosphatase catalytic subunit–related protein-specific CD8+ T cells. ...

[This] led to substantial, long-term protection against autoimmune diabetes ... 

These data present a proof of principle that IL-35 could be used as a potent inhibitor of autoimmune diabetes and implicate its potential therapeutic utility in the treatment of type 1 diabetes.

Abstract: http://diabetes.diabetesjournals.org/content/early/2012/03/13/db11-0784.short

CD40 inhibitory peptide by Wagner at University of Colorado

Quotes:

Wagner isolated the specific T-cells that attack the pancreas and cause most cases of Type 1 Diabetes. The research team has developed a drug that attacks those bad cells. 

It’s having an impressive effect on mice. The drug is not only preventing mice from developing diabetes, it’s also reversing the effects of diabetes in mice that already have the disease.

News article: http://denver.cbslocal.com/2012/03/09/cu-researchers-find-cure-for-type-1-diabetes-in-mice/

Related grant: http://www.diabetes.org/news-research/research/research-database/cd40-as-a-biomarker-in-type-1-diabetes.html
Related research: http://www.jleukbio.org/content/84/2/431.abstract

XMetA by Bhaskar at XOMA

XMetA is the first antibody specific for the insulin receptor shown to correct hyperglycemia in a mouse model of diabetes. Results of a study conducted by XOMA and confirmed by investigators at the University of California, San Francisco, demonstrate that XMetA has the potential to be a novel, long-acting agent for the control of blood glucose levels in patients with diabetes.
The study by Bhaskar, et al. demonstrated that XMetA markedly reduced elevated fasting blood glucose levels and normalized glucose tolerance in mice experimentally rendered diabetic. After six weeks of treatment, there was a statistically significant reduction in hemoglobin A1c levels in animals treated with XMetA compared to controls (p < 0.05). In addition, elevated non-HDL cholesterol levels were improved relative to control mice (p < 0.05). Hypoglycemia and weight gain were not observed during this study, nor was proliferation of cell growth.


Press Release: http://www.sciencecodex.com/first_allosteric_insulin_receptoractivating_antibody_to_improve_glycemic_control_in_vivo-87483
Abstract: http://www.ncbi.nlm.nih.gov/pubmed?term=Bhaskar%20XMetA

Hepatic Insulin by Elsner at

The plan for this research was to genetically engineer a virus to create insulin, and then inject that virus into the liver of diabetic animals.  The result was normal BG for the one year duration of the trial.

Title: Reversal of Diabetes Through Gene Therapy of Diabetic Rats by Hepatic Insulin Expression via Lentiviral Transduction

Quotes from Abstract:

• Within 5–7 days after the virus injection of 7 × 109INS-lentiviral particles the blood glucose concentrations were normalized in the treated animals. 
• This glucose lowering effect remained stable for the 1 year observation period. 
• Human C-peptide as a marker for hepatic release of human insulin was in the range of 50–100 pmol/ml serum.
• This study shows that the diabetic state can be efficiently reversed by insulin release from non-endocrine cells through a somatic gene therapy approach.

Two different types of animals were used:

• autoimmune-diabetic IDDM rats (LEW.1AR1/Ztm-iddm) 
• streptozotocin-diabetic rats

Abstract: http://www.ncbi.nlm.nih.gov/pubmed/22354377

Brown Adipose Tissue Transplant by Gunawardana at Vanderbilt University

Title: Reversal of Type 1 Diabetes in Mice by Brown Adipose Tissue Transplant

Quote from the abstract:

Here, we show that subcutaneous transplants of embryonic brown adipose tissue (BAT) can correct T1D in streptozotocin-treated mice (both immune competent and immune deficient) ... BAT transplants result in euglycemia, normalized glucose tolerance, reduced tissue inflammation, and reversal of clinical diabetes markers such as polyuria, polydipsia, and polyphagia.

Abstract: http://diabetes.diabetesjournals.org/content/61/3/674.short

News coverage: http://news.vanderbilt.edu/2012/03/fat-as-diabetes-treatment/

anti-CD98hc by Lian at University of Tokushima

Paper Title: Manipulation of CD98 resolves type 1 diabetes in nonobese diabetic mice.

Quote from the Abstract:

Injection of the anti-CD98hc [monoclonal antibody] completely prevented the onset of cyclophosphamide-induced diabetes in NOD mice. Treatment of diabetic NOD mice with anti-CD98hc reversed the diabetic state to normal levels, .... Furthermore, treatment of diabetic NOD mice with CD98hc small interfering RNA resolved T1D. These data indicate that strategies targeting CD98hc might have clinical application for treating T1D

Abstract: http://www.ncbi.nlm.nih.gov/pubmed/22291182

Protein and Nanoparticle by Santamaria at Parvus

Quote:

Parvus, which is basically Santamaria, Coggins and Jord Cowan and two of them still have day jobs has spent the last 18 months testing the treatment on mice.
With 70 per cent to 80 per cent of the animals permanently free of diabetes after receiving the injections, according to Coggins, the company is now looking to raise $30 million to move to clinical trials.
Even the 20 to 30 per cent of mice who relapse see the disease disappear after another round of treatment, Coggins said.

News article: http://www.calgaryherald.com/touch/story.html?id=6064209