New insights into diabetic blindness

April 9, 2010, University College Dublin
New insights into diabetic blindness
Retinal vasculature of an adult transgenic (Fli1:EGFP) zebrafish. After 30 days of hyperglycaemia, these vessels display many of the abnormal features observed in the retinal capillaries of diabetic patients.

( -- New research by University College Dublin scientists indicates that treatment of diabetic blindness should look at protecting the neurons responsible for colour vision in the eye and not just targeting the blood vessels as is currently the practice.

The research team led by Conway Fellow, Dr Breandán Kennedy from the School of Biomolecular & Biomedical Science recently published their findings in the journal Disease Models & Mechanisms.

Nearly 2.5 million people worldwide are blind due to a secondary complication of diabetes called diabetic retinopathy. This disorder activates the growth of new leaky in the eye and is responsible for the death of photoreceptors, the neurons that send visual messages to our brain.

Until now, scientists were unclear if the changes to vessels and neurons occurred independently of one other. Questions were also asked about which type of retinal neuron is most likely to die as a result of the raised glucose levels seen in diabetes.

Dr Kennedy and his team found that new blood vessels and the neuronal cell death in diabetic retinopathy can arise independently of each other. In addition, they identified that cone photoreceptor neurons, those involved in and which we use to see during daylight are most affected by the high glucose levels.

The research team made their observations by successfully generating a zebrafish model of diabetes. The eyes of these small, tropical freshwater fish are very similar in design to humans, making it a useful species to study blindness. The high levels of glucose typically seen in people suffering with diabetes were stimulated in zebrafish and the fish studied to see whether they exhibited known diabetic symptoms.

This novel model of the disease resembles the early stages of diabetic retinopathy in humans. It is an exciting development for the Kennedy group who now hope to further extend their research and establish a model of late stage diabetic disease.

Current treatment for diabetic retinopathy sufferers tries to prevent the growth of new blood vessels in the late stage of the disease. There are associated side effects and the treatments halt but do not cure the disease. This research suggests a need to also protect the neurons before the disease progresses to the late stage.

Commenting on the research, Dr Kennedy said, “By establishing a robust model for early and late stage diabetic retinopathy, we would hope to better understand the progression of the disease and pave the way for identifying new drug targets for its successful treatment”.

Related Stories

Recommended for you

Past encounters with the flu shape vaccine response

February 20, 2018
New research on why the influenza vaccine was only modestly effective in recent years shows that immune history with the flu influences a person's response to the vaccine.

Building better tiny kidneys to test drugs and help people avoid dialysis

February 16, 2018
A free online kidney atlas built by USC researchers empowers stem cell scientists everywhere to generate more human-like tiny kidneys for testing new drugs and creating renal replacement therapies.

Expanding Hepatitis C testing to all adults is cost-effective and improves outcomes

February 16, 2018
According to a new study, screening all adults for hepatitis C (HCV) is a cost-effective way to improve clinical outcomes of HCV and identify more infected people compared to current recommendations. Using a simulation model, ...

Study suggests expanded range for emerging tick-borne disease

February 16, 2018
Human cases of Borrelia miyamotoi, a tick-borne infection with some similarities to Lyme disease, were discovered in the eastern United States less than a decade ago. Now new research led by the Yale School of Public Health ...

Flu shot only 36 percent effective, making bad year worse (Update)

February 15, 2018
The flu vaccine is doing a poor job protecting older Americans and others against the bug that's causing most illnesses.

IFN-mediated immunity to influenza A virus infection influenced by RIPK3 protein

February 15, 2018
Each year, influenza kills half a million people globally with the elderly and very young most often the victims. In fact, the Centers for Disease Control and Prevention reported 37 children have died in the United States ...

1 comment

Adjust slider to filter visible comments by rank

Display comments: newest first

not rated yet Apr 11, 2010
One might wonder exactly WHAT these researchers ARE studying when they MISS all the iron in the eye. It is well known iron in the eye destroys it. It is also well known there is MORE iron in the eye of a diabetic than is KNOWN to harm the eye but yet they FAIL to target this iron. How can someone KNOW something will destroy something and THEN fail to react TO that substance ? Stupidity is the only answer.

RESULTS: The level of vitreous iron
increased threefold in Eales' disease (1.85 +/- 0.36 pg/ml), 2.5-fold in
proliferative diabetic retinopathy (1.534 +/- 0.17 pg/ml) and 2.3-fold in eyes
with intraocular foreign body (1.341 +/- 0.25 pg/ml) when compared with macular
hole (0.588 +/- 0.16 pg/ml).

This suggests
that the least amount of ferrous ions necessary to cause liquefaction
of the rabbit vitreous is in the range of 16.8 to 39.2 micrograms of
elemental iron, a concentration of 0.3 to 0.7 mM in the vitreous.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.