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

Catenarin by Shen at Taiwan

Quote from Abstract:

Overall, the data demonstrate the preventive effect and molecular mechanism of action of catenarin on T1D, suggesting its novel use as a prophylactic agent in T1D.

Abstract: http://www.hindawi.com/journals/ecam/2012/982396/abs/
Full paper: http://downloads.hindawi.com/journals/ecam/2012/982396.pdf

heparan sulfate by Simeonovic at The Australian National University

Quotes:

Scientists suggest that either boosting pancreatic islet levels of heparan sulfate (HS) or administering an inhibitor of the heparanase enzyme that is responsible for its breakdown could provide a new approach to preventing development or slowing progression of type 1 diabetes. A team at The Australian National University’s John Curtin School of Medical Research initially showed that HS is expressed at very high levels in the mouse islet and is essential for β-cell survival.

Charmaine J. Simeonovic, M.D., and colleagues, report their findings in The Journal of Clinical Investigation, in a paper titled “Heparan sulfate and heparanase play key roles in mouse β cell survival and autoimmune diabetes.”

Critically, treating prediabetic female MOD mice using PI-88, at an age when they were expected to exhibit both NDI and DI, significantly slowed the development of T1D by 10 weeks. By age 36 weeks, the number of diabetic mice among the PI-88 cohort was just half that of the control group.

http://www.genengnews.com/gen-news-highlights/researchers-find-approach-to-hold-type-1-diabetes-back/81246103/

Encapsulated Beta Cells by Nuvilex at SG Austria

Quote from the press release:

Nuvilex, Inc.announced today their affiliate SG Austria and partners have successfully treated diabetes in an established, recognized animal model utilizing live encapsulated cells.

The introduced cells responded to elevated blood sugar levels by producing insulin, alleviating the symptoms of diabetes. Moreover, encapsulated cells remained viable and responsive for many months.

Press release: http://www.marketwatch.com/story/nuvilex-and-sg-austria-introduce-revolutionary-treatment-for-diabetes-utilizing-live-cell-encapsulation-technology-2011-12-06