New study finds ways to treat insulin resistance in type 2 diabetes
Release date: 2016-11-07
A team of researchers led by researchers at the University of California School of Medicine can reverse diabetes insulin resistance and glucose intolerance in an obese diabetic mouse model by eliminating the protein galectin-3 (Gal3).
By binding to the insulin receptor on the cell, Gal3 prevents insulin resistance caused by insulin binding to the receptor. A team led by Professor Jerrold Olefsky from the Department of Endocrinology and Metabolism Medicine at the University of California, San Diego School of Medicine, showed that insulin sensitivity and glucose tolerance can be restored even in older mice by genetically deleting Gal3 or using drug inhibitors. normal. However, obese mice remained unchanged.
"This study uses Gal3 as a target for insulin resistance and diabetes in a mouse model," Olefsky, deputy director of scientific affairs at the study's senior author. "Our findings suggest that Gal3 inhibition in humans may be an effective treatment for diabetes."
Olefsky and other researchers have been studying how chronic tissue inflammation leads to insulin resistance in type 2 diabetes. In an article published in the Cellular Journal on November 3, the researchers explained that inflammation requires specific endoproses that destroy target cells. For example, in obese adipose tissue (fat), 40% of the cells are macrophages. Macrophages also secrete lectin-3 and then act as a signaling protein to attract more macrophages, leading to more Gal3 production.
In addition, the researchers identified macrophages derived from bone marrow as a source of Gal3 that causes insulin resistance. More importantly, the researchers found that Gal3 is secreted by macrophages and can cause insulin resistance in liver, fat cells, and muscle cells independent of inflammation.
Gal3 has been linked to other diseases. Olefsky will continue research on Gal3 loss that may be a target for nonalcoholic steatohepatitis and treatment of heart and liver fibrosis.
Source: Noble
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