Brown adipose tissue in a woman shown in the FDG PET/CT . test

Research shows that boosting a protein concentrated in brown adipose tissue regenerates white adipose tissue to reduce diabetes risk.

A new study led by UT Southwestern scientists shows that increasing the amount of protein concentrated in brown fat can lower blood sugar, promote insulin sensitivity and protect against fatty liver disease by regenerate white fat into a healthier state. Findings published online on Nature Communications magazine, which could eventually lead to new solutions for patients with diabetes and related diseases.

Lead researcher Perry E. Bickel, MD, associate professor of internal medicine at UTSW, said: “By leveraging this natural system, we can help make trans fat stores healthier and more efficient. have the potential to prevent or treat obesity-associated diabetes.”

Tens of millions of Americans have Type 2 diabetes, a disease characterized by high blood sugar and resistance to insulin, the hormone that allows cells to use blood sugar for energy. The disease is linked to obesity, with excess white adipose tissue (WAT) – the fatty tissue that holds most of the body’s energy stores – linked to elevated blood sugar and insulin resistance in sensitive individuals. Humans and other mammals also have a second type of fat, called brown adipose tissue (BAT), that burns fat as a way to increase body temperature at temperatures cold. BAT has been studied as a potential target for weight loss, Bickel says, but may also have a role in improving blood sugar independent of weight loss.

In the study, Bickel and his colleagues, including co-leader Violeta I. Gallardo-Montejano, MD, an instructor at UTSW, found that brown fat may play an important role in preserving protect against diabetes. The researchers discovered this while studying perilipin 5 (PLIN5), a protein that coats lipid droplets inside cells, especially in BAT.

When the team genetically engineered more PLIN5 in the BAT, the animals maintained significantly lower blood sugar levels and higher insulin sensitivity in the glucose tolerance tests, compared with mice that did not. normal PLIN5 levels. They also had less fatty liver, a condition linked to type 2 diabetes.

Looking for the mechanism behind these positive changes, the scientists discovered that the mitochondria of BAT in the transgenic mice were adapted to burn more fat, similar to what was seen in animals. The object is placed in cold temperature. However, adaptation was not sufficient to explain the hypoglycemic effect. Taking a closer look, the researchers found that the white fat cells of the animals with added PLIN5 in their brown fat cells were smaller and reduced several markers of inflammation — changes that have been linked to improved cellulite. insulin sensitivity and sugar metabolism.

Bickel notes that BAT appears to communicate with WAT in some unspecified way, potentially sending a molecular factor through the bloodstream when PLIN5 levels rise inside brown fat cells.

“The next question we want to address is what that factor is and whether we can exploit it for therapeutic benefit,” says Bickel.

The study was funded by grants from the National Institutes of Health (R01DK115875, R01DK112826 and R01DK108833) and the Wayne State University Entrepreneurship fund.

Other researchers who contributed to this study include the late Chaofeng Yang and Lisa Hahner of UTSW, Joshua A. Johnson, John L. McAfee of the Cleveland Clinic, William L. Holland of the University of Utah, and Rodrigo Fernandez-Valdivia of Wayne State University School of Medicine.

Bickel in association with Daniel W. Foster, Physician, Chair of Excellence in Internal Medicine.

Source: https://www.sciencedaily.com/releases/2021/06/210604122453.htm

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Translated by: Thu Vo