Key cause of type 2 diabetes uncovered

[Amity Island]

Glucose metabolites (chemicals produced when glucose is broken down by cells), rather than glucose itself, have been discovered to be key to the progression of type 2 diabetes. In diabetes, the pancreatic beta-cells do not release enough of the hormone insulin, which lowers blood glucose levels. This is because a glucose metabolite damages pancreatic beta-cell function.]

Key cause of type 2 diabetes uncovered | University of Oxford

Oxford Research reveals high blood glucose reprograms the metabolism of pancreatic beta-cells in diabetes.

www.ox.ac.uk

 

[Leadinglights]

I do find it annoying that they show a picture of a blood glucose monitor showing units in mg/dl which is not what we use in the UK.
This seems to go against the insulin resistance theory which suggests the pancreas actually produces too much insulin but it is not being used effectively.

 

[harbottle]

This is not really about insulin resistance. It's about the beta cell dysfunction that is part of T2 diabetes.

The insulin resistance causes hyperinsulinemia (Higher than normal levels of insulin) during the pre-diabetic stages of the diseases in order to cope with the increase in blood glucose due to the resistance. Once diabetes has been reached, some of the beta cells have stopped working (As the paper says, up to 50% of insulin production can be lost). This paper pretty shows a potential reason for this dysfunction and it's due to the high levels of glucose, leading to endless spiral in which the higher and longer blood sugar is high, the more damage is done.

If euglycaemia is quickly restored, these changes will rapidly reverse. However, changes in metabolic gene/protein expression induced by prolonged hyperglycaemia will not be so rapidly reversed and their accumulation may lead to the development of impaired glucose intolerance (IGT). Once IGT is established, we postulate it initiates a vicious spiral in which elevated plasma glucose impairs β-cell metabolism and insulin secretion further, causing greater hyperglycaemia and fuelling the progression of IGT to diabetes. As little as 8 mM glucose appears to be sufficient to initiate this cycle in human islets

This section appears to indicate how important it is to act during the pre-diabetic stage, as the damage can be reversed. Also the longer blood sugar has been elevated, the reversal isn't as quick.

Doesn't this tie in with the observations with the Newcastle work? There was, over the space of a year or more, a slow improvement in insulin levels in response to blood sugar levels.

 

[Deleted member 21371]

This is not really about insulin resistance. It's about the beta cell dysfunction that is part of T2 diabetes.

The insulin resistance causes hyperinsulinemia (Higher than normal levels of insulin) during the pre-diabetic stages of the diseases in order to cope with the increase in blood glucose due to the resistance. Once diabetes has been reached, some of the beta cells have stopped working (As the paper says, up to 50% of insulin production can be lost). This paper pretty shows a potential reason for this dysfunction and it's due to the high levels of glucose, leading to endless spiral in which the higher and longer blood sugar is high, the more damage is done.



This section appears to indicate how important it is to act during the pre-diabetic stage, as the damage can be reversed. Also the longer blood sugar has been elevated, the reversal isn't as quick.

Doesn't this tie in with the observations with the Newcastle work? There was, over the space of a year or more, a slow improvement in insulin levels in response to blood sugar levels.

It does seem that the speed of the action can make a difference then.
It does seem the fast weight loss leads to a reversal, a slower weight loss seems to need to be followed by a regime of diet control.

 

[AndBreathe]

How many people diagnosed with T2 have had their insulin production measured or assessed? I'd wager very few.

 

[harbottle]

I know they did it for the Newcastle work, as the paper shows the graphics that indicate first phase and second phase insulin production returned to normal levels for 'responders'.