Pioneering research on type 2 diabetes

[Northerner]

While legions of medical researchers have been looking to understand the genetic basis of disease and how mutations may affect human health, a group of biomedical researchers at UC Santa Barbara is studying the metabolism of cells and their surrounding tissue, to ferret out ways in which certain diseases begin. This approach, which includes computer modeling, can be applied to type 2 diabetes, autoimmune diseases, and neurodegenerative diseases, among others.

Scientists at UC Santa Barbara have published groundbreaking results of a study of type 2 diabetes that point to changes in cellular metabolism as the triggering factor for the disease, rather than genetic predisposition. Type 2 diabetes is a chronic condition in which blood sugar or glucose levels are high. It affects a large and growing segment of the human population, especially among the obese. The team of scientists expects the discovery to become a basis for efforts to prevent and cure this disease.

http://www.universityofcalifornia.edu/news/article/28888

 

[mcdonagh47]

While legions of medical researchers have been looking to understand the genetic basis of disease and how mutations may affect human health, a group of biomedical researchers at UC Santa Barbara is studying the metabolism of cells and their surrounding tissue, to ferret out ways in which certain diseases begin. This approach, which includes computer modeling, can be applied to type 2 diabetes, autoimmune diseases, and neurodegenerative diseases, among others.

Scientists at UC Santa Barbara have published groundbreaking results of a study of type 2 diabetes that point to changes in cellular metabolism as the triggering factor for the disease, rather than genetic predisposition. Type 2 diabetes is a chronic condition in which blood sugar or glucose levels are high. It affects a large and growing segment of the human population, especially among the obese. The team of scientists expects the discovery to become a basis for efforts to prevent and cure this disease.

http://www.universityofcalifornia.edu/news/article/28888

The article seems to say something that runs counter to most of what we have been told i.e. T2 is associated with Insulin Resistance and the bodies of T2s at diagnosis are awash with unused insulin. This report seems to say the opposite i.e. that poor insulin production is the problem ....the downgrading of the genetic background in this report is also new ...

"Normally, beta cells in the pancreas sense a rise in blood sugar and then secrete insulin to regulate blood glucose levels. But in type 2 diabetes, the beta cells fail to execute this important function and blood sugar rises, a trend that can reach life-threatening levels. The researchers identified a "tipping point," or metabolic threshold, that when crossed results in the failure of beta cells to adequately sense glucose in order to properly secrete insulin."

The report also confirms the link between Obesity and Type 2.

 

[Northerner]

I would be interested to know what a C-peptide test would show in a newly-diagnosed T2. My consultant said a healthy, non-diabetic person would normally produce about 20 units a day - surely a test would show whether a person was producing considerably more which was then being 'resisted' or if it was a case of insulin insufficiency?

 

[Vicsetter]

From what T2s have said on this board I would have thought that some people have increased resistance, some don't produce enough insulin and a wide variation in between. It is fairly obvious that a number of us inject massive quantities of insulin with very little effect (I'm back at 120 units a day at the moment) so it must be insulin resistance that is affecting me.

 

[Mark T]

It's a shame the NHS doesn't do a standard batch of tests including the more common antibodies, c-peptide, etc. But I suppose it's a cost issue.

I've always read that Type 2 is a combination of insulin resistance and insulin secretion defect. But most new research that I've read seems to focus on insulin resistance only.

Perhaps at some point someone will define Type X for a specific issue that causes the insulin secretion defect? There are a few of us that don't fit into the typical model.

Of course the question that specific article didn't seem to say is; what causes the changes in cellular metabolism?

 

[trophywench]

Well I thought as well as insulin resistance, rather than producing not enough insulin, what happened with some T2s was they lose their Phase 1 insulin production, ie food in mouth - enzymes in saliva (ptyalin, pepsin) discover food, start digesting it and it starts to be absorbed through the inside of the cheeks at which point the Pancreas is alerted and Insulin production starts, that's the Phase 1 bit. Then when the body considers whats being eaten in greater details ie once it actually fully gets into the bloodstream, it produces just enough to cope and Bob's your uncle.

Except with lack of Phase 1, with it being on catch-up anyway cos the Phase 2 started too late, it's fighting a losing battle - and continues to do so cos of IR - hence the old 'little and often' dietary advice and why they now advise slowly absorbed carbs for T2s anyway.

Then your Pancreas gets knackered from overwork and just can't keep up at all so there you are - injecting gallons of insulin to keep going.