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Liver inflammation discovery could explain vascular complications risk in diabetes

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German researchers have unlocked a previously unknown mechanism as to why people with diabetes have a higher risk of long-term complications. Scientists have identified inflammatory processes in the liver which increase cholesterol in people with diabetes. This, researchers believe, could promote the development of vascular diseases. They also discovered a molecule called GAbp (GA-binding protein) which provides a protective effect against vascular diseases, and could be important in preventing complications. "Our data suggest that the liver plays a key role in the development of common diabetic vascular diseases," said first author Dr. Katharina Niopek, researcher at the Institute for Diabetes and Cancer (IDC) at Helmholtz Zentrum Minchen. "GAbp appears to be a molecular regulator at the interface between inflammation, cholesterol homeostasis and atherosclerosis. Without its protective effect, this leads to hypercholesterolemia and increased lipid deposition in the arteries." The researchers had aimed to identify why people with diabetes who have good blood glucose control were still at a higher risk of complications compared to those without the condition. They examined inflammatory processes in type 2 diabetes and obesity, which both contribute to long-term complications, and demonstrated that inflammation caused by metabolic disorders increases the production reactive oxygen species (ROS) in the liver. When ROS production is heightened, this prevents GAbp from working, leading to greater levels of cholesterol and symptoms of atherosclerosis. "Since initial patient data supported our findings, the new signalling pathway - regardless of how well the blood glucose levels of the patient are controlled - may be a key component in the development of long-term diabetes complications which could be utilized therapeutically," added lead author Professor Stephan Herzig. The study has been published in the journal Cell Reports.

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INFLAMMATION again! Insulin resistance at it's worse. I have low levels of inflammation but very high IR so I'm told by endocrologist.
But inflammation causes asthma, joint pain and atherosclerosis in me.

Cure inflammation and millions will live a more pain free life! Including diabetics.
 
Given that one drug that was designed to reduce inflammation was discoved unexpativtly in the clincal test to help with Type2, I expect will will hear a lot more about inflammation being linked ot Type2 over the next few years.

Thes standard blood tests for inflammation may not pick up the not yet understood type of inflammation that is connected to some or all insulin resistance. I also expect the IR may remain even after the inflammation has gone.
 
Given that one drug that was designed to reduce inflammation was discoved unexpativtly in the clincal test to help with Type2, I expect will will hear a lot more about inflammation being linked ot Type2 over the next few years.

Thes standard blood tests for inflammation may not pick up the not yet understood type of inflammation that is connected to some or all insulin resistance. I also expect the IR may remain even after the inflammation has gone.
I bet. IR is the cause.
Which, originally needed for type2, drug has aided inflammation?
 
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