On November 29, the reporter learned from Jinan University (hereinafter referred to as Jinan University) that Professor Yin Zhinan's team of biomedical Transformation Research Institute of Jinan University found for the first time that interleukin (IL-27) can directly target adipocytes, promote adipocyte heat production, burn lipids, consume calories and easily lose weight. More importantly, IL-27 can improve type 2 diabetes and provide new targets and potential drugs for the treatment of obesity and related metabolic diseases. Recently, the journal Nature published this research achievement online. "Insulin resistance is not only a cause of obesity, but also a series of metabolic diseases, including type 2 diabetes, fatty liver and ovarian polycystic syndrome. If we can improve insulin resistance, obesity and many metabolic diseases may lead to a better therapeutic approach," Yin Zhinan said. Yin Zhinan has been engaged in basic and clinical research on immunity and health for a long time. In 2014, he proposed to study obesity from the perspective of the immune system to see whether it can bring new ways and new hope to obesity treatment from the perspective of the immune system. "Through clinical observation, we found that the content of IL-27 in obese patients was low, but after they completed weight loss surgery, the level of IL-27 returned to normal." Yin Zhinan said that he and the team were particularly curious about whether IL-27, a specific targeted immune cell in the traditional concept, could be a new target for weight loss? The team constructed a variety of genetically engineered mice, adopted the obesity model induced by high-fat diet, and combined with the samples of obese people. It was found that the level of IL-27 in the serum of obese people would indeed decrease. This study found for the first time that IL-27 can cause browning of white adipocytes and activate "fat combustion" by directly acting on adipocytes; By changing the lipid in adipose tissue into heat, it can reduce body weight and improve metabolic diseases such as diabetes. This study breaks through the traditional concept of IL-27 specifically targeting immune cells. In animal experiments, injection of recombinant IL-27 can significantly reduce the weight of obese mice and improve their insulin signal sensitivity, which preliminarily verified the potential of IL-27 as a therapeutic drug. "The fundamental reason why type 2 diabetes is difficult to overcome is that the response of the insulin signal is weakened. Insulin is like a key. The whole signal to respond to it is a lock. If the lock is rusted, the key will be inserted into it, and it will not be able to open the lock for half a day." Wang Qian, the first author of the paper and the postdoctoral fellow of Zhuhai People's Hospital affiliated to Beijing University, said: "We now find that the role of IL-27 is equivalent to making the keyhole more lubricated, so that the key can be unlocked as soon as it is put in, so as to improve the overall disorder of patients and restore their blood glucose to a healthy level." Because IL-27 is a molecule that is normally expressed in the body, not a synthetic exogenous compound, it is safe. "It can improve the type 2 diabetes, burn fat, reduce weight and improve the sensitivity of insulin signal response on the mechanism without restricting diet and without dieting." Another first author of the paper, Li Dehai, postdoctoral fellow of Zhuhai People's Hospital Affiliated to Jinan University. "We look forward to the industrialization of this therapeutic target as soon as possible, to promote its clinical application, to develop RNA related drugs, and to provide a brand new treatment for obesity, diabetes, fatty liver and other metabolic diseases." Yin also revealed another research direction to predict the health status through changes in IL-27 levels. However, he also stressed that there is still a long way to go from laboratory to clinic, which requires the joint efforts of policies, investment and other aspects. (outlook new era)
Edit：Yuanqi Tang Responsible editor：Xiao Yu
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