Type 1 Diabetes a Nerve Disease?
Type 1 Diabetes a Nerve Disease?
Findings in Mice Suggest Totally New Direction for Diabetes Treatment
By Daniel J. DeNoon
WebMD Medical News
Reviewed by Louise Chang, MD
Dec. 18, 2006 -- Sensory nerve cells -- not immune cells -- may be the key culprits in type 1 diabetes, mouse studies suggest.
The findings, if confirmed in humans, would turn diabetes research on its head. They suggest that diabetes could be treated or prevented with drugs that work on the nervous system.
The study is published in the Dec. 15 issue of Cell; it comes from the labs of Hans Michael Dosch, MD, PhD, and Michael Salter, MD, PhD, at The Hospital for Sick Children in Toronto.
"We are now working hard to extend our studies to [type 1 diabetes] patients, where many have sensory nerve abnormalities," Dosch says in a news release. "But we don't yet know if these abnormalities start early in life and if they contribute to disease development."
Type 1 Diabetes a Nerve Defect?
Most researchers believe type 1 diabetes is a problem with the immune system attacking healthy cells.
These new findings suggest that haywire immune responses are tied to defective sensory nerve cells.
These cells, called TRPV1 neurons, respond to insulin by sending out powerful chemical signals, one of which is a pain-related protein called substance P.
Dosch and Salter's team finds that in diabetic mice, TRPV1 neurons send only a weak signal. When the researchers killed off the mice's TRPV1 cells, the animals' diabetes disappeared. And when they injected the animals' pancreases with substance P, most became diabetes-free.
The researchers suggest that defective sensory nerves help start -- and maintain -- diabetes in diabetes-prone humans.
"Our observations open new avenues for therapeutic strategies," Dosch, Salter, and colleagues conclude.
They also say TRPV1 defects may play a role in other autoimmune diseases. Lupus and rheumatoid arthritis are examples of other autoimmune diseases.
An editorial by University of California researchers Helene Bour-Jordan, PhD, and Jeffrey A. Bluestone, PhD, accompanies the Dosch and Salter team's report.
Bour-Jordan and Bluestone say the new findings support a growing suspicion among researchers that autoimmune diseases arise from interplays between the nervous system and the immune system.
Type 1 Diabetes a Nerve Disease?
Findings in Mice Suggest Totally New Direction for Diabetes Treatment
By Daniel J. DeNoon
WebMD Medical News
Reviewed by Louise Chang, MD
Dec. 18, 2006 -- Sensory nerve cells -- not immune cells -- may be the key culprits in type 1 diabetes, mouse studies suggest.
The findings, if confirmed in humans, would turn diabetes research on its head. They suggest that diabetes could be treated or prevented with drugs that work on the nervous system.
The study is published in the Dec. 15 issue of Cell; it comes from the labs of Hans Michael Dosch, MD, PhD, and Michael Salter, MD, PhD, at The Hospital for Sick Children in Toronto.
"We are now working hard to extend our studies to [type 1 diabetes] patients, where many have sensory nerve abnormalities," Dosch says in a news release. "But we don't yet know if these abnormalities start early in life and if they contribute to disease development."
Type 1 Diabetes a Nerve Defect?
Most researchers believe type 1 diabetes is a problem with the immune system attacking healthy cells.
These new findings suggest that haywire immune responses are tied to defective sensory nerve cells.
These cells, called TRPV1 neurons, respond to insulin by sending out powerful chemical signals, one of which is a pain-related protein called substance P.
Dosch and Salter's team finds that in diabetic mice, TRPV1 neurons send only a weak signal. When the researchers killed off the mice's TRPV1 cells, the animals' diabetes disappeared. And when they injected the animals' pancreases with substance P, most became diabetes-free.
The researchers suggest that defective sensory nerves help start -- and maintain -- diabetes in diabetes-prone humans.
"Our observations open new avenues for therapeutic strategies," Dosch, Salter, and colleagues conclude.
They also say TRPV1 defects may play a role in other autoimmune diseases. Lupus and rheumatoid arthritis are examples of other autoimmune diseases.
An editorial by University of California researchers Helene Bour-Jordan, PhD, and Jeffrey A. Bluestone, PhD, accompanies the Dosch and Salter team's report.
Bour-Jordan and Bluestone say the new findings support a growing suspicion among researchers that autoimmune diseases arise from interplays between the nervous system and the immune system.
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