Amiline and the possible cure of diabetes

It seems interesting ...

August 26, 2014 • News Diabetes, Home

A new study has found that type 1 diabetes and type 2 diabetes are the result of the same mechanism, specifically the formation of toxic lumps of a hormone called amiline.A thesis that breaks with the idea of ​​treating the two types of diabetes in different ways.In the amiline the common link of both diseases could be.

The results, based on 20 years of work in New Zealand, suggest that type 1 diabetes and type 2 could potentially be reversed through medications that stop the formation of these toxic amiline groups.

In addition to producing insulin, pancreas cells also produce another hormone called amiline.Insulin and amiline normally work together to regulate body response to food intake.If they no longer occur, then blood sugar levels as we know rise causing diabetes and causing long -term damage in target organs such as heart, kidneys, eyes for example.Hence the good glycemic control is the key.

Returning to amiline, we now know that it occurs around the pancreas cells and that in its toxic version destroys the cells that produce insulin.The consequence of this cell death is diabetes.

An earlier investigation suggested that this is the mechanism causing type 2 diabetes. This new research provides strong evidence that type 1 diabetes develops equally.The difference is that the disease begins at an earlier age and progresses more rapidly in type 1 compared to type 2 because there is a faster deposition of toxic aggregates of the amiline in the pancreas.

Professor Garth Cooper at Manchester said they hope to have potential medications ready to enter clinical trials in the next two years.These tests are expected to be carried out shortly in patients type 1 and type 2. These clinical trials are planning with research groups in England and Scotland.

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How interesting this research, the problem to what leads me and I am almost convinced is that, our cure does not really interest, I obviously refer to pharmacists and the system, a clear example of continuous glucose measurement devices or the pumps of pumps themselvesInsulin infusion.
For many opinions about them there is not a single user that the device has been harmful.
The truth is a shame ...

Anicordoba, totally agree with you.But hopefully things can change and we can see this solution for diabetes.

As always, people who know how to read scientific magazines give a very different vision of this news to which the media give:

Amylin is a hormone which is both needy and potentially pathological, since it plays an essential role in a wide Range of Normal Physiological Process, But when it clumps Together it can produces toxic Fibers Which, Among Other Things, Damage The Pancreatic Beta Cells.The Useful Things It Does Include Limiting The Appetite, Influencing The Sensation of Thirst, Slowing The Rate of Gastric Emtying, Inhibiting The Production of Glucagon, Promoting Bone Metabolism, interacting with neurons which play a Role in Energy Balance, and assisting vasodilation, so thereis no way to do without it.Since ITS ABILITY TO SLOW THE PROCESSING OF FOOD, REDUCE APPETITE, AND PROMOTE VASODILATION SUGGESTS THAT IT WOULD BE HELPFUL IN TREATING DIABETES, IT HAS BEEN USED FOR A LONG TIME EXPERIMENTALL IN DIABETIC MEDICINE.But Given That Increased Amounts of It Can Cause Amylin Aggregations Which Damage Beta Cells, It You have needed to use Substance, Pramlintide, Which Acts Like Amylin Without This Side-Effect.It has even Been Given to Type 1 Diabetics Along With Insulin, and It Was Aable to Achieve A Minor Reduction in Hba1c Values, From an average of 8.9% without it to 8.6% with it.

The particular Experiment Under Discuse in these News Reports Studied Mice Bred to have a gene causing excess production of Amylin.The Homozygous Mice Suf Seraced A Rapid Loss of Pancreatic Beta Cells Analogous to Type 1 Diabetes in Humans.The hemizygous mice experienced a lot of gradual loss of pancreatic Beta Cells with increased age, analogous to type 2 diabetes in humans.(1)

So the results are not as impressive as the press reports suggest.First, The Experiment Was Drivers In Mice, which Never Serve As a Vry Good Model of Human Diabetes, and They Were Artificially Genetically Modified Mice.Second, Finding to Cause SelDom Leads Vary Directly to Identifying a Cure for Anything in Medicine.What we have here is one possessible model for what is Happening in Human Diabetes, Which Will No Doubt Inspire Further Lines of Research, but not Really Any Any Immediate Solution.

1) S. Zhang, et al, "The Pathogenic Mechanism of Diabetes Varies with the Degree of Oligomerization of Human Amylin and Pancreatic Islet Beta Cells," The Faseb Journal, vol.28, no.8, 19 August, 2014.

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Thanks for the text @Sherpa41, I translate from English the part of the conclusions, to simplify reading, it would be the following:

So the results are not as impressive as the reports published in the press suggest.

What we have here is a possible model of what happens in human diabetes, which will undoubtedly inspire new lines of research, but it is not really an immediate solution.

Here the original text:

So the results are not as impressive as the press reports suggest.First, The Experiment Was Drivers In Mice, which Never Serve As a Vry Good Model of Human Diabetes, and They Were Artificially Genetically Modified Mice.Second, Finding to Cause SelDom Leads Vary Directly to Identifying a Cure for Anything in Medicine.What we have here is one possessible model for what is Happening in Human Diabetes, Which Will No Doubt Inspire Further Lines of Research, but not Really Any Any Immediate Solution.

Anicordoba said:
How interesting this research, the problem to what takes me and I am almost convinced is that, our cure does not really interest, I obviously refer to pharmacists and the system, a clear example the measurement devicesContinuous glucose or insulin infusion pumps themselves.
For many opinions about them there is not a single user that the device has been harmful.
The truth is a shame ...

I think exactly the same.