A team led by researchers at the University of California School of Medicine was able to reverse diabetes insulin resistance and impaired glucose tolerance by eliminating protein galectin-3 (Gal3) in obese diabetic mouse models and using recombinant human proteins.
By binding to the insulin receptor on the cell, Gal3 prevents insulin from binding to the receptor-induced insulin resistance. A team led by Professor Jerrold Olefsky, professor of endocrine and metabolic medicine from the University of California, San Diego School of Medicine, showed that by gene deletion Gal3 or using a drug inhibitor, insulin sensitivity and glucose tolerance can be restored even in older mice normal. However, obese mice remained unchanged.
"This study used Gal3 as a program target for insulin resistance and diabetes in the mouse model," said Olefsky, senior director of the study, a deputy director of scientific research. "Our findings suggest that Gal3 inhibition in the human body may be an effective treatment for diabetes."
Olefsky and other researchers have been studying how chronic tissue inflammation leads to type 2 diabetes insulin resistance. In an article published in a cell journal on November 3, the researchers explained that inflammation needs to disrupt the specific exclusive macrophages of target cells. For example, in obese adipose tissue (fat), 40% of the cells are macrophages. Macrophages also secrete lactose lectin - 3, and then as a signal protein to attract more macrophages, resulting in more Gal3 production.
In addition, the researchers identified the source of bone marrow macrophages that are the source of insulin resistance that leads to insulin resistance. More importantly, the researchers found that Gal3 is secreted by macrophages and can lead to insulin resistance independent of inflammation in the liver, adipocytes and muscle cells.
Gal3 has been linked to other diseases. Olefsky would continue to study Gal3 depletion that may serve as a target for nonalcoholic steatohepatitis and heart and liver fibrosis. By the way, Flarebio offers high-quality recombinant proteins and antibodies such as PODXL Monoclonal Antibody.
Many people who are overweight or who have diabetes, prediabetes, or high cholesterol may also have liver damage without knowing it. Nonalcoholic steatohepatitis (NASH) is a liver disease that occurs when a buildup of fat in the liver causes irritation (inflammation) and damage that may interfere with how the liver works. Many people with NASH feel fine and do not even know they have the condition.
回复删除If you have been told that you have or may have either NASH or a fatty liver, and diet and exercise haven’t worked, you may want to consider participation in the VIA clinical research study.
What is the purpose of the VIA clinical research study?
The VIA study is evaluating whether a once-daily, oral investigational medication called volixibat, is tolerable, safe, and effective in reducing liver damage in people with NASH. The study will evaluate the effects (if any) of three different doses of volixibat in patients with NASH.
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