“Preventing Type 2 Diabetes and Insulin Resistance: Promising Research demonstrates the Crucial Role of Cortisone Receptors in Scavenger Cells, paving the way for Better Diagnosis and Treatment Options”

by time news

2023-05-05 03:30:19

More and more people are suffering from type 2 diabetes. This usually comes with insulin resistance. What if you could prevent that?

More and more obese people worldwide are getting Typ-2-Diabetes. Before diabetes develops, those affected first develop one due to chronic inflammation of the adipose tissue insulin resistance as a precursor.

Researchers led by Prof. Jan Tuckermann from the Institute for Molecular Endocrinology of Animals at the University of Ulm have now demonstrated in a mouse model that insulin resistance increases when scavenger cells lack certain cortisone receptors. This basic research could lead to better diagnostic options and optimized treatment of insulin resistance. The German-Danish Study was published in the specialist publication Nature Communications published.

The scavenger cells and diabetes

With increasing prosperity and the availability of high-calorie foods, type 2 diabetes is also spreading in emerging countries. The WHO estimates that the number of people with diabetes almost quadrupled between 1980 and 2014, from 108 to 422 million. “But not all obese people are automatically insulin resistant,” says Tuckermann. The subject of his research is which endogenous factors can protect against insulin resistance.

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With such resistance, the pancreas insulin to lower the blood sugar level, but the hormone can no longer work properly. Because the message that sugar has to be absorbed from the blood and taken into the cells no longer reaches the responsible glucose transporters, and insulin is less effective. How can one prevent the development of type 2 diabetes, which often results from insulin resistance?

The resistances have to give way

Insulin resistance is caused by a chronic, low-threshold inflammatory reaction in adipose tissue. Inflammation occurs when too many macrophages in adipose tissue to eliminate dead cells. “In the mouse model, we were able to show that the glucocorticoid receptor in scavenger cells in adipose tissue is crucial for suppressing inflammation and thus for avoiding diet-related insulin resistance,” say the study’s two first authors, Giorgio Caratti and Ulrich Stifel.

Glucocorticoid are cortisol-like, highly anti-inflammatory hormones that act directly in the macrophages. The researchers conducted their study on mice that were fed a high-calorie diet and were very overweight, whose adipose tissue was subclinically inflamed and which had been genetically modified in such a way that they lacked the glucocorticoid receptor in scavenger cells. The body’s own anti-inflammatory substances could therefore no longer dock there and have an effect on the cells.

The scientists demonstrated that the loss of the receptor in mice leads to more inflammation in adipose tissue and more pronounced insulin resistance than in unmodified animals. In addition, the researchers conducted animal-free experiments with tissue cultures. “It’s difficult to do research like this completely outside of the animal,” explains Tuckermann. Because: “Cortisone works throughout the body.” The results still have to be validated in humans.

What does this mean for therapy?

Another unexpected result: “The glucocorticoid receptor is not solely responsible for the anti-inflammatory effects, but is also strongly dependent on the signaling protein STAT 6, which also has an anti-inflammatory effect,” emphasizes Dr. Alexander Rauch from the University of Southern Denmark.

What does this mean for the diagnosis and treatment of insulin resistance in humans? “If we succeed in bringing cortisone to these macrophages in obese people in a cell-specific manner, it could be possible to reduce insulin resistance,” says Tuckermann. The basic research may also result in new diagnostic options: Thin mice have more glucocorticoid receptors in macrophages and therefore less insulin resistance. “We think it could be similar in humans.”

This article is based on a press release of the University of Ulm. We have the original publication for you here and linked in the text.

Image source: Maksim Shutov, unsplash

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