From Our 2010 Archives
Mouse Study Sheds Light on Diabetes-Heart Disease Link
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In the new study, published in the June 24 issue of the journal Neuron, the investigators found that high blood sugar prevents critical communication between the brain and the autonomic nervous system, which controls involuntary activities in the body.
"Diseases, such as diabetes, that disturb the function of the autonomic nervous system cause a wide range of abnormalities that include poor control of blood pressure, cardiac arrhythmias and digestive problems," senior author Dr. Ellis Cooper, of McGill University in Montreal, explained in a news release from the journal's publisher. "In most people with diabetes, the malfunction of the autonomic nervous system adversely affects their quality of life and shortens life expectancy."
For the study, Cooper and his colleagues used mice with a form of diabetes to examine electrical signal transmission from the brain to autonomic neurons. This communication occurs at synapses, which are small gaps between neurons where electrical signals are relayed cell-to-cell via chemical neurotransmitters.
"In healthy individuals, synaptic transmission in the autonomic nervous system is strong and stable; however, if synapses on these neurons malfunction due to some disease process, the link between the nervous system and the periphery becomes disrupted," Cooper said in the news release.
The researchers found that, in mice, high blood sugar elevates reactive molecules that contain the oxygen atom (called reactive oxygen species) in autonomic neurons. This chemical change inactivates the neurotransmitter receptors at these synapses, they noted.
"Our work provides a new explanation for diabetic-induced disruptions of the autonomic nervous system," Cooper said. "This synaptic depression is apparent as early as one week after the onset of diabetes and becomes more severe over time."
It's important to note that animal studies, while an important part of the scientific process, often fail to yield similar results in humans.
-- Robert Preidt
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SOURCE: Cell Press, news release, June 23, 2010