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Recently, "Cell" magazine published the latest research results of the team of Professor Li Pingping, the national key laboratory of natural drug active substances and functions of the Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College: Galectin-3 (Gal3) as a link Key molecules of obesity, inflammation and IR play an important role in the pathogenesis of diabetes. This study suggests that chronic inflammation leads to a new mechanism of IR that provides new drug targets for the treatment of diabetes.
The IR and diabetes caused by obesity are on a global scale. China currently has the largest number of people with diabetes, and the number of cases has increased year by year. However, the pathogenesis of IR and diabetes has not yet been elucidated.
IR is a function of insulin to regulate blood sugar, and the body secretes excessively high insulin for controlling blood sugar levels. The body is diagnosed with diabetes after decompensation. The Li Pingping team has long been committed to the research of the immunological mechanism of IR. Previous studies have suggested that chronic inflammation induced by Cd11c macrophages can directly lead to IR, and Cd11c macrophages from obese mice contain large amounts of Galectin-3.
Li Pingping team first discovered that Gal3 induced IR in macrophages, and elaborated the molecular mechanism of Gal3 regulation of IR. The study found that the levels of Gal3 in the blood of obese mice fed a high-fat diet were abnormally elevated. Gal3 acts directly on the three major target organs of insulin: inhibits insulin-mediated glucose uptake in muscle and adipose tissue; induces hepatic glucose production. Further studies have found that Gal3 binds to the glycosylated insulin receptor via the C-terminal carbohydrate recognition region, reducing its tyrosine phosphorylation, thereby interfering with the insulin signaling pathway and ultimately leading to IR. The study also found that blood levels of Gal3 were significantly increased in obese patients, while Gal3 induced IR in human muscle cells. Targeting Gal3 found that both the knockout of the Gal3 gene and the administration of Gal3 inhibitors significantly improved IR in obese mice. These results suggest that Gal3 may be a potential molecular drug target for IR and diabetes.
Scientists have discovered that chronic inflammation leads to new IR mechanisms that help treat diabetes
[China Pharmaceutical Network Industry News] Studies have shown that Galectin-3 (Gal3), a key molecule that links obesity, inflammation and IR, plays an important role in the pathogenesis of diabetes. This study suggests that chronic inflammation leads to a new mechanism of IR that provides new drug targets for the treatment of diabetes.