Interesting Lloyd. This makes it all that much more important to start insulin earlier to try and preserve Beta cell function. Controlling BG with insulin while having some remaining beta cell function is easier than doing it with none at all.
I do not agree with that statement as it tends to suggest that T2 islets are dying.
Yes I agree that T2 islets do see insulin production decline but there is some research and argument that the islets in too much glucose and oxidation products seem to go into a rip van winkle state that under removal of the excess bloodstream glucose and oxidation products recover production of insulin on T2's.
Work done on cadaver islets of T2's when put back into more normal glucose levels and oxidation products have shown return to production of insulin.
Work done at University of Newcastle Upon Tyne using MRI spectography of folks on extreme low diets have shown islet recovery as in bariatric sugery patients.
T1's do sho outright islet loss and destruction.
I believe science is stuck on some wrong ideas and thinking here! I do not disagree with the concept of using insulin to reduce any further stress and give T2 islets a break! The oral pills glyburide/starlix, glimperide et all are a dead loss in this area and I had been on them in part of my 30 year hiatus as a type 2.
I do agree with you Jims up to a point. I believe there comes a point when islet cell cannot be brought back. It has been shown that they do sometimes recover when the conditions are made right but I have I believe made my conditions right. I have lost weight down to a recommended BMI, I exercise and I maintain a moderately low carb diet but still there has been no change in insulin needs in two years other than the reduction I noticed when going on my pump which is common.
I believe your statement is true for some but the saying that "Your diabetes may vary" applies here.
Stemwinder(Gary):
Thank you very much for commenting. The problem is that we do not have sufficient science and data on why Type 2 islets have a possibility of recovery action and what the possibilities are and how much actual destruction in type 2's occur. University of Newcastle and another group have recorded this recovery watching pancreas islets as well as watching liver operation on the MRI Spectography
For me after 26 years with my body with excess glucose and poor iset function, I cannot explain why my islets came back on the job after getting the excess glucose burned off and out of my body, getting excess liver glucose release arrested by metformin and using a 1200 calorie diet to reduce excess glucose release from ingested food and making the glucose burn rate more match the available glucose from food and organ sources.
I as one case count for nothing but the science on T2 Diabetes has to take into account the whole body operation of a multi-organ system and get beyond this simplistic one organ thinking on what causes T2 diabetes.
In addition, the human body uses a distributed storage system of the skeletal muscles to store excess glucose from the blood system And those stores are not infinite and how such a distributed system uses insulin signalling to enable the skeletal muscles with space to take up more glucose while those fully loaded ignore the insulin. The science in this area is poor, inadequate and ignored.
My ignorant guess is that in order to recover islets if that is possible requires the backing down and removal of excess glucose flooding the body and overloading the skeletal muscle stores.
My own case is a curious case in point. I spent 26 years with numbers too high and eventually had stroke and numbers crawling thru the roof.
Too much of what is considered T2 science is a direct transfer from extensive type 1 research which I do believe is accurate in that T1 environment. No discussion.
What I cannot resolve in my mind is the following:
a) bariatric surgery and extreme 600 calorie diet work done by University of Newcastle Upon Tyne using MRI spectography have shown pancreatic islet recovery and going back to work.
b) research work in Italy looking at cadavers and their islets from type 2's and normal folks showed something curious where they were looking for differences in the islets of the two types but could not with the tools they had uncover any major differences. They then put type 2 islets into normal glucose operating/oxidation products solutions and the type 2 islets went back and made insulin unexpectedly.
c) others have reported islet recovery as well under curious circumstances.
I had the benefit of running on a cgms for a year and a half when my own islets came back on the job totally unexpectedly. A miracle - no but:
After 6 months after getting glucose numbers hauled back, liver excess glucose release arrested using metformin , diet cut back to 1200 calories - modified low cal and extra exercise - 2 miles walking a day; I start seeing curious behavior on the cgms:
a) As I am eating I start seeing a drop on the cgms as a bolus from pancreas is now showing up - un explained. Confirmed on caveman fingerprick machine.
b) suddenly in one week I am seeing extreme lows on my cgms that made no sense. I immediately started cutting out 1/2 dose of starlix at meals - not enough. Then I removed the whole dose of starlix.
c) I had been on 26 units of 75/25 to help stop dawn phen ( many years I might add). I was continuing to get extreme lows and started cutting that back and called my Doctor about all this curious low activity; he put me on 6 units dose of Humalog Lispro U-100.
d) I continued to reduce those doses to the low activity to about 1 to 2 units per meal as needed.
e) at same time I had been on lantus for last 6 months for about 12 units per day and that ended up being reduced to 2 units and dropped.
f) today , I am on my 1200 calorie diet and 2 miles walking and doses of metformin ( 500mg); and 1 to 2 units of Humalog lispro as needed at each meal. Actos was booted. The CGMS was crucial to prevent extreme lows during this period of a couple of weeks.
In the end, whether T2 islets have the possibility to recover their use and action or whether they have been destroyed is in my mind unproven, not known and honestly needs some serious science using mri spectography to clarify this matter.
In addition the science of glucose flow control to muscles and how the human body deals with constant overload of glucose from diet, excess liver glucose release and other bodily misfires needs proper science on that as well.