Pancreas size changes when type 2's go into remission

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Just to be clear, the study suggests that pancreas size decreases as part of T2D, and then grows again with remission.

Resolves an open question from the DiRECT study - ie is a small pancreas a sign that somebody is predisposed to T2D, or is it a result of T2D.
 
Just to be clear, the study suggests that pancreas size decreases as part of T2D, and then grows again with remission.

Resolves an open question from the DiRECT study - ie is a small pancreas a sign that somebody is predisposed to T2D, or is it a result of T2D.
Still not addressing those that don't achieve reversal!
 
Just to be clear, the study suggests that pancreas size decreases as part of T2D, and then grows again with remission.

Resolves an open question from the DiRECT study - ie is a small pancreas a sign that somebody is predisposed to T2D, or is it a result of T2D.
Eddy,
Well explained.
 
I also read about this recently. We are often told that the word 'remission' is the preferred term because your T2 can return, and other terms like 'reversing Type 2 diabetes' incorrectly suggests you're cured. If normal pancreatic function could resume after 2 years in remission that would be truly amazing result, but would someone then be considered to be cured I wonder?

Martin

The pancreas rebooting (in many cases) after weight loss was the big finding of the DiRECT study.

I call this a "cure".
 
More colour on this study: https://www.medscape.com/viewarticle/937977#vp_1


Prof Taylor said in his presentation of the results that the 50% loss of beta cell function in type 2 diabetes patients "has been reproduced by many studies using different methodologies, and often coupled with the gloomy message: It goes downhill, always".


"Well, here, we can see it going uphill, not just uphill but entirely back to normal, and with maintained weight it remained normal up to the 24 months of DiRECT."


In the post-presentation debate, Dr Harald Sourij, Medical University of Graz, Austria, asked Professor Taylor about the mechanism by which pancreatic morphology and volume was restored in these patients.


"We have to remember that insulin is a very potent stimulator of growth," Prof Taylor replied.


He pointed out that insulin and insulin-like growth factor 1 "have identical effects on their respective receptors, at about a 10-fold difference in concentration".


"Now consider insulin," he said. "After a meal, your plasma insulin will rise up to 10-fold from baseline. Just imagine what the local concentration is around the islet. That must be fairly considerable."


Prof Taylor continued: "The trophic effect of insulin is probably the most likely reason for this [normalisation of pancreatic morphology].


"We’re seeing a return to normal of parenchymal cells of the pancreas and I would just draw your attention to the fact that when insulin secretion is lost in that very different condition, type 1 diabetes…then the pancreas also shrinks.


"By the time of the presentation of type 1 diabetes, it is about 30% of normal size. So perhaps we shouldn’t be surprised, knowing that the acute response to meals in type 2 diabetes is very poor, that the pancreas may shrink because of the lack of the continuing trophic effects of insulin."
 
Sounds like nonsense to me. The pancreas is mainly there to provide digestive enzymes. The beta cells producing insulin occupy a tiny volume.

The pancreas can be surrounded by fat, so losing weight may give the impression that the pancreas is changing size. In fact, the pancreas hardly ever changes in size other than shrinking due to chronic pancreatitis - my pancreas sure is, it’s heavily calcified and atrophic.
 
Sounds like nonsense to me. The pancreas is mainly there to provide digestive enzymes. The beta cells producing insulin occupy a tiny volume.

The pancreas can be surrounded by fat, so losing weight may give the impression that the pancreas is changing size. In fact, the pancreas hardly ever changes in size other than shrinking due to chronic pancreatitis - my pancreas sure is, it’s heavily calcified and atrophic.

No idea, really, but it doesn't seem to be complete nonsense. Eg: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5497047/
 
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