Los Angeles | Genetically removing a protein or using drugs to target it may reverse diabetic insulin resistance and glucose intolerance, a new study in mice suggests.
By binding to insulin receptors on cells, the protein Galectin-3 (Gal3) prevents insulin from attaching to the receptors resulting in cellular insulin resistance.
Researchers from the University of California San Diego in the US, showed that by genetically removing Gal3 or using pharmaceutical inhibitors to target it, insulin sensitivity and glucose tolerance could be returned to normal, even among older mice. However, obesity remained unchanged.
“This study puts Gal3 on the map for insulin resistance and diabetes in mouse model. Our findings suggest that Gal3 inhibition in people could be an effective anti-diabetic approach,” said Jerrold Olefsky, professor at UC San Diego.
Olefsky and other researchers have been studying how chronic tissue inflammation leads to insulin resistance in type 2 diabetes.
Researchers explain that inflammation requires macrophages – specialised cells that destroy targeted cells.
In obese adipose tissue (fat), for example, 40 per cent of cells are macrophages.
Macrophages in turn secrete Gal3, which then acts as a signalling protein attracting more macrophages, thus resulting in the production of even more Gal3.
Researchers also identified bone marrow-derived macrophages as the source of Gal3 that leads to insulin resistance.
They found that Gal3 is secreted by macrophages and can then cause insulin resistance in liver, fat cells and muscle cells independent of inflammation.
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