Originally Posted by mcdonagh47
You DO suddenly become dxed Type 2 Diabetic when Insulin Resistance outweighs Beta Cell Mass as plotted against each other on the Starling Curve of the Pancreas.
Beta cell death is certainly a major factor in T2 and there has been a big reduction in beta cells by the time someone has developed impaired fasting glycemia.(prediabetes)
At the Mayo clinic they looked at pancreases (pancreata?) of a number of subjects immediatley after death.
http://diabetes.diabetesjournals.org/content/52/1/102.full
People who were
obese, but not T2 had a 50% greater beta cell volume than people who were lean and not diabetic. So obese non diabetics have the capacity to produce more insulin.
Those who were obese and had
T2 had 63% less beta cell volume than non diabetic obese controls
Those who were obese and had
impaired fasting glycemia had 40% less volume than non diabetic obese controls.
Those who were
lean and had T2 had 41% less volume than lean non diabetic controls.
(it was the number of cells, not the size of the cells that made the diffference in volume)
They looked at the
apoptosis,( programmed cell death) and
replication (increase following division) of the beta cells.
Apoptosis was slightly, but
not significantly greater in obese diabetics than obese non diabetics. It
was significantly greater in lean diabetics than lean non diabetics.
BUT as those with diabetes had a smaller volume of cells in the first place.
There was a relative
3 fold increase in the frequency of apoptosis in obese diabetics compared with obese non diabetics
There was a
10 fold increase in the frequency of apoptosis in lean diabetics compared with lean non diabetics.
Replication was the same in all cases, obese or lean, diabetic or non diabetic , it occurred but it was
slow and it declined with age.
Reversal as well as increasing insulin sensitivity would have to include being able to stop this rate of death and increase the number of beta cells so sufficient insulin can be produced at all times, not just with a reduced carbohydrate intake. Otherwise when there was a big demand on insulin as for example in some illnesses there might not be enough production capability.
A major problem is that cell replication is slow and declines with age.
It is possible that new islets are formed elsewhere and when this paper was written in 2003 they were optimistic as the site they thought new cells were produced was normal. They said that they had found the the presence of islets budding from exocrine ducts in all pancreata irrespective of obesity or diabetic status. As I understand it, they thought new cells were able to be formed in these ducts.
Unfortunately, the juries out on this one. Recently other researchers have found what they say is proof that new beta cells are not formed in the exocrine ducts after birth