Many new T2D related studies have been piling up during the last 6 weeks, and I have been struggling in selecting the most interesting ones, not to mention trying to actually understand them. Four of them made it.
Week 28 – A new study provides new insight on preventing blindness caused by diabetic eye complications
When diabteic edema, an abnormal build up of tissue fluid starts affecting the eye, it starts a damaging domino effect in the retina. It goes something like this:
Blockage blood flow in one vessel -> local drop of oxygen -> stimulates production of growth factor protein (VEGF) -> reinforces further blockages
Normally VEGF is a key factor for new blood vessel growth, but with elevated blood glucose in the retina it causes vessel blockages to propagate.
The study provides a virtual model of the retina, which helps predicting the rate and pattern of this damage cascade. Based on a patient´s retinal vascular structure, probability calculations are made to create a personalized map of strategic points to target in laser therapy.
“Our analysis suggests treatment of the retina with a large number of very small laser burns could prevent this ‘domino-like’ progressive loss of small retinal blood vessels and prevent elevation of VEGF and the major complications of diabetic retinopathy,” – Thomas Gast, ophthalmologist and senior scientist, IU School of Optometry
Week 29 – Study suggests that diabetes could be caused by the failure of a few ‘privileged’ beta cells
Instead of depending on all beta cells in the pancreas, the synthesis and secretion of insulin could be dictated by certain hubs of specialised beta cells.
The study at Imperial College London was done using optogenetic and photopharmacological methods on pancreatic islets from rats and humans. In these types of studies the signalling pathways of modified cells are controlled with light, and in this study it was done in order to map the glucose response hierarchy of beta cells. When the function of certain beta cells was turned off, their islets stopped responding to glucose. The percentage of these ‘conductor’ beta cells was deteremined to be as little as 1-10% of all beta cells.
“It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion. These findings provide a revised blueprint for how our pancreatic islets function, whereby these hubs dictate the behaviour of other cells in response to glucose.” – Dr David Hodson, University of Birmingham
This insight into the roles of beta cells could pave way for new precision therapies that target these crtical hubs in the pancreas.
Week 32 – Scientists have discovered a new link between muscle fat accumulation and insulin resistance
A protein that functions as DNA binder and transcription activator in glucose related gene regulation, MondoA. It is a key factor in whether muscle cells burn or store fat, normally turning a oversupply of glucose into stored fat. An excessive fat coversion rate will, however, turn the function of MondoA more into insulin signalling inhibition.
The research at Sanford-Burnham Prebys Medical Discovery Institute focused on the main insulin responder of the body, skeletal muscle. The team considers MondoA as a potential blocking target for treating early stage T2D.
Week 33 – Another protein linked to T2D
Another T2D related protein discovery that gives a new clue to understanding the link between accumulated fat and insulin resistance. The lack of protein PTRF Cavin-1 causes loss of fat cells, which in turn causes mistargeting of fat, supposedly promoting insulin resistance.
An abundance of fat cells should therefore, in principle, protect from insulin resistance. However, overburdening of Cells in making new PTRF in response to excessive nutrition might be the reason why fat cell loss would happen even in obese individuals.