Re: Diabetes breakthrough in mice; Article Two, posted twice!

I was just going to post that here too!! [Ya beat me to it]

Some thoughts :
- since there is neurological damage, and since neurological damage is most often caused by neurotoxins [duh!], I believe we have uncovered yet another disease of the modern plague - chemical toxins in our environment, in our diet, in our clothes, in our water and in our pancreas.

- the news that by just giving one shot to take out the problem of these particular sensory nerves and thereby stopping the insulin shortage is great stuff - but bad news for the "insulin products suppliers" who will probably do all they can to see that this treatment never sees the light of day.

- Question: Is this "Substance P" mentioned here the same as the Substance P that they found in chronic pain victims? If chronic pain people do not get diabetis as often as the rest of the population, this could be why?




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here is a similiar article from New Scientist:

http://tinyurl.com/yxrz4z


"Breakthrough sheds light on cause of diabetes"

* 17:56 15 December 2006
* NewScientist.com news service

"One of the root causes of type 1 diabetes may need rethinking – the condition may be triggered by faulty nerves in the pancreas, a new study reveals.

Type 1 diabetes has long been described as an autoimmune disease in which the body’s immune system targets islet cells in the pancreas, eventually destroying their ability to produce insulin. Without insulin, the body cannot convert glucose into energy, so people with type 1 diabetes have to regularly inject themselves with insulin to survive.

However, what initiates the original attack on the pancreas had been unclear. It now seems that the nervous system may play a key role, according to researchers in Toronto, Canada. The team eliminated the disease in diabetes-prone mice by knocking out a set of faulty sensory nerves. They believe the finding could chart a new path in treatment of the disease in humans.

Michael Dosch at the Hospital for Sick Children in Toronto, and colleagues, had previously shown that not only islet cells, but the nerve tissue around them was affected as diabetes set in. For this reason, they suspected that certain sensory nerves of the pancreas might be involved. These nerves release a neuropeptide called "substance P" and are usually responsible for ensuring that islet cells produce the right amount of insulin.

The researchers used a chemical to obliterate these nerves in a breed of mice genetically predestined to develop diabetes. “It turns out if you remove these specific sensory nerves, the animals don’t get diabetes,” says Dosch. “It was stunning.”
Single injection

When the researchers examined the nerves of diabetes-prone mice and compared them with normal mice, they found that the nerves of diabetes-prone mice do not producing enough substance P. This causes islet cells to overproduce insulin, leading to insulin-resistance and eventually islet-cell death. It is at this point, says Dosch, that the immune system is called into action, triggering diabetes.

The team wanted to know what would happen if they gave diabetic mice a top-up of substance P, so they injected some directly into the pancreas. Astonishingly, the diabetes disappeared overnight and the mice remained diabetes-free for weeks, and even months in some cases.

If the same were to happen in humans, a single injection could keep the disease at bay for years, says Dosch.
Other mechanisms

“These are interesting and original observations, and could potentially open new avenues for diabetes therapies,” says David Leslie of the Centre for Diabetes and Metabolic Medicine at Barts and The London, Queen Mary’s School of Medicine and Dentistry in London, UK.

The findings also support previous suggestions of a possible connection between autoimmunity and the nervous system. However, “there are almost certainly other mechanisms by which these mice, and indeed humans, get type 1 diabetes,” Leslie says.

About 85% of human diabetics are believed to have impaired sensory nerve function, but it has always been assumed to be a consequence of the disease, rather than a cause, says Dosch.

"This work merits serious consideration,” says Matt Hunt, Science Information Manager at Diabetes UK. However, since the study was carried out on specific neurons in mice, “future work in human populations with high rates of type 1 diabetes, such as Scandinavia, would seem a possible area to pursue," he adds.

From January 2007, Dosch plans to look for evidence of sensory abnormalities in babies born to high-risk families, and will follow them to see if impairment is predictive of disease.

Journal reference: Cell (vol 127, p 1123) Tweet