Using mouse models of obesity and diabetes, researchers showed that genetically removing Gal3 or targeting it with pharmaceutical inhibitors allows insulin sensitivity and glucose tolerance to return to normal.
When chronic tissue inflammation occurs, it requires macrophages — specialized cells that destroy targeted cells. Macrophages secrete Gal3, which then acts as a signaling protein attracting more macrophages. Gal3 binds to insulin receptors on cells, and prevents insulin from attaching to the receptors, which causes insulin resistance.
“This study puts Gal3 on the map for insulin resistance and diabetes in mouse model,” said Jerrold Olefsky, MD, professor of medicine in the endocrinology and metabolism division at La Jolla, Calif.-based UC San Diego School of Medicine and senior author of the study. “Our findings suggest that Gal3 inhibition in people could be an effective anti-diabetic approach.”
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