JDRF - Juvenile Diabetes Research Foundation

Serotonin is commonly known as “the happy hormone” for its role in managing and moderating human behavior and mood but a recent discovery by JDRF scientists have shown that it also plays a rather different role – triggering the growth of new beta cells in pregnant women.

It’s been known for a while that women can produce new beta cells to allow for the increase in insulin needed to supply energy during pregnancy but how this happens has been a mystery. In an exciting new discovery, a team of JDRF researchers have identified key steps in this process and shown that serotonin is one of the triggers.

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JDRF researchers from Canada show that a new vaccine can cure type 1 diabetes in mice and slow the onset of the condition in mice at risk of the disease.

Type 1 diabetes is caused when a persons own immune system attacks and destroys the insulin-producing cells in the pancreas. Whilst the precise trigger of this attack is still unproven, researchers do know that there are certain immune cells that play a more important role than others. The challenge is to target the “bad” cells without harming the good cells that protect us from day-to-day infections.

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JDRF researchers have shown for the first time that other pancreas cells can spontaneously re-program themselves to produce insulin without the need for complex genetic modification or surgical transplantation.

Under healthy conditions, beta cells regenerate slowly to respond to increased insulin requirements or to replace those lost by injury. In the case of type 1 diabetes however, the beta cells are destroyed faster than they can naturally regenerate.

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JDRF funded research in the US has found that a hormone associated with the body’s fight or flight instinct prompts beta cells to grow and to produce insulin.

These findings reinforce the potential of regeneration as a cure for diabetes and provide insights for discovering new approaches to treat people with diabetes by restoring or regenerating their ability to produce insulin.

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A JDRF-funded clinical trial has shown that a drug used to treat certain types of cancer can protect beta cells, and therefore preserve insulin production, in people newly diagnosed with type 1 diabetes.

The trial, conducted in the US through the international Type 1 Diabetes TrialNet consortium and published in the New England Journal of Medicine, provides the first conclusive evidence that it is possible to target particular types of immune cells to reduce or prevent the onset of type 1 diabetes.

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A move towards individualised insulin therapy targets

After extensive discussion in Australia and overseas, Australian diabetes health professionals have released a new position statement on blood sugar targets for people with type 1 diabetes. Following the results of the Diabetes Control and Complications trial, the ideal target of a HbA1c of 7% was set across the board.

Recent research has suggested that one size may not fit all and to address this, the Australian Diabetes Society now officially recommends that people with severe hypoglycemia or hypoglycemia unawareness should set their HbA1c targets at 8% or less.

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European researchers have successfully converted pancreas cells into insulin-producing beta cells by altering a single gene.

In a major finding that adds to the prospects of regenerating insulin-producing tissue in people with type 1 diabetes, JDRF-funded researchers have shown that beta cells can be made using another type of pancreas cell by simply turning on a specific gene called PAX4.

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New York, NY, August 6, 2009 — In findings that add to the prospects of regenerating insulin-producing cells in people with type 1 diabetes, researchers in Europe — co-funded by the Juvenile Diabetes Research Foundation — have shown that insulin-producing beta cells can be derived from non-insulin-producing cells in the pancreas.

In results of a study published today in the journal Cell, the researchers, led by Patrick Collombat of the Max-Planck Institute for Biophysical Chemistry in Germany and Ahmed Mansouri of the University of Göttingen in Germany, in collaboration with researchers at the JDRF Center for Beta Cell Therapy in Diabetes in Brussels, discovered in mice that new insulin-producing beta cells can be generated from alpha cells in the islets of the pancreas by modifying the expression of a specific gene (Pax4) in alpha cells. (Alpha cells generate the hormone glucagon in response to low blood sugar to restore normal blood sugar levels.)  They also discovered that the alpha cells that give rise to new beta cells originate from progenitor cells in the pancreas. The newly formed beta cells result in better glucose control and prolonged survival of younger mice with diabetes.

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For many years, researchers have suspected that bacteria, viruses and other micro-organisms play an important role in the development of autoimmune conditions such as type 1 diabetes. This “hygiene hypothesis” postulates that our decreasing exposure to a lower amount of bugs and germs may leave some people more susceptible to autoimmune attacks.

A team of researchers from Yale University in the US have leant further support to this hypothesis by demonstrating that a certain strain of research mice were far more likely to develop type 1 diabetes when raised in a special germ-free environment as opposed to normal laboratory conditions.

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A recent study shows that a new type of stem cell transplantation may help people with type 1 diabetes become insulin free and increase C-peptide levels.

Researchers have used a transplant of a patient’s own treated blood cells to increase and preserve beta cell function in young people recently diagnosed with type 1 diabetes.

The research team, from the US and Brazil, hoped that if they intervened early enough they could wipe out and then rebuild the body’s immune system by using stem cells, preserving a reservoir of beta cells and allowing them to regenerate.

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