JDRF Research
6. Regenerating Islets in the Body
Existing pancreatic beta cells, not adult stem cells, replicate to replace old or damaged cells.
In May 2004, JDRF-funded researchers at Harvard University and the Howard Hughes Medical Institute reported a landmark discovery about how the body makes new insulin-secreting cells in the pancreas to replace those lost by normal aging, injury, or disease. The scientists found that new beta cells are formed through the replication of existing beta cells rather than the differentiation of adult stem cells. The finding, made in mice, suggests that the body’s capacity to make copies of pancreatic beta cells might be boosted by medical treatments, allowing patients with type 1 diabetes to regenerate the cells and regain control of blood sugar levels. It also establishes firmly that adult stem cells in the pancreas do not contribute to new beta cell formation in this mouse model. Yuval Dor, Ph.D., recipient of a JDRF postdoctoral fellowship, led the study, conducted in the laboratory of JDRF-funded researcher Douglas Melton, Ph.D.
7. Researchers Identify Diabetes Susceptibility Gene
Gene identification may help identify children at risk for type 1 diabetes.
In July 2004, JDRF-funded researchers at the Medical College of Georgia identified a gene that in a certain form may increase the risk of juvenile (type 1) diabetes. The discovery could improve screening for disease susceptibility to help identify children at risk, and it confirms a pathway that may be implicated in the development of the disease. The gene, called SUMO-4, helps regulate the intensity of the immune response so that it does not attack the body’s own tissue. One variant, or allele, of SUMO-4 does not carry out its task properly. When SUMO-4 has this particular variant, the immune system loses a natural brake and becomes more “reactive” to environmental triggers. This may increase its chance of mistakenly attacking the beta cells in the pancreas.
8. Boosting Certain Immune Cells to Block Diabetes
Animal study shows that cell therapy may stop the immune system attack that leads to type 1 diabetes.
In June 2004, JDRF-funded researchers at Rockefeller University reported halting type 1 diabetes by using one type of immune cell, the dendritic cell, to stimulate expansion of another, the suppressor T cell. The resulting increase in the number of suppressor T cells shut down the immune attack against the pancreatic islets and stopped the disease. The study, conducted in mice, suggests it may be possible to retrain a malfunctioning immune system by expanding the number of suppressor T cells outside the body and them reintroducing them. The work was led by Kristin Tarbell, Ph.D., recipient of a JDRF postdoctoral fellowship grant.
9. T Cell Reaction May Explain Autoimmune Response
Immune cell finding changes the way researchers look at type 1 prevention strategies.
Research reported in February 2004 suggested that the misguided immune attack leading to type 1 diabetes may be due to the manner in which immune T cells react after first being exposed to islet cell antigens that cause the disease. The finding may alter researchers' strategies to prevent the development of type 1 diabetes. Many scientists had assumed that the disease was caused by a unique group of T cells reacting aggressively to an islet antigen, but the current study suggests that the crucial factor is how the T cells respond. The researchers found that T cells in people without type 1 diabetes also respond to islet antigens, but theirs is a immunoregulatory or immune tolerance (i.e., defensive) response, while someone with type 1 diabetes launches a destructive response. The discovery was made by Mark Peakman, Ph.D., and colleagues at King’s College London, in the United Kingdom, and published in the February issue of the Journal of Clinical Investigation.
10. Enzyme Plays Big Role in Complications
Discovery of enzyme associated with blood vessel damage and drug-development efforts aimed at blocking the enzyme’s action may help prevent serious diabetic complications.
Although technically a 2003 discovery, the PARP enzyme made big waves in diabetes research in 2004. In October 2003, Michael Brownlee, M.D., a JDRF-funded researcher at the Albert Einstein College of Medicine, identified an enzyme that plays a key role in the blood vessel damage that often affects people with diabetes. The enzyme, called PARP (for poly ADP-ribose) causes damage to blood vessels that can lead to diabetic retinopathy, neuropathy, and nephropathy. In November 2003, a JDRF-funded research study at the University of California at San Francisco reported that a new class of drugs blocking PARP’s action can prevent the brain damage that often results from hypoglycemia. After receiving the drugs––called PARP inhibitors––diabetic rats that had been in hypoglycemic comas experienced up to 90 percent reductions in brain cell death compared with a control group of animals. Significantly, the drugs appear to be effective in animals even if given up to two hours after hypoglycemia has been reversed.
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