糖尿病,脂肪肝 z-bo 2020-10-08 319

　　The prevalence of fatty liver among Chinese urban residents is as high as 27%, and one quarter of urban residents suffer from alcoholic or non-alcoholic fatty liver. At the same time, the prevalence of type 2 diabetes in China has risen rapidly in the past few decades. According to the latest data in 2020, the prevalence of diabetes in China's adult population is 12.8%, and nearly half of adults have abnormal blood sugar levels. In recent years, scholars have found that the risk of diabetes in fatty liver patients is significantly higher than that in non-fatty liver patients, but the mechanism is not fully understood. Scientists at the University of Copenhagen (University of Copenhagen) published a molecular metabolism study in September and found that glucagon secreted by pancreatic islet alpha cells can quickly regulate amino acid metabolism in the liver.

　　This connection between the pancreas and the liver disrupts the fat production of the liver and produces "glucagon resistance". This may be the reason why patients with fatty liver are prone to diabetes, and it also provides new ideas for the prevention and treatment of diabetes. In this study, the researchers found that under normal circumstances, normal glucagon function directly affects the plasma amino acid clearance and urea production in mice. Through transcriptome analysis, a series of genes related to this phenomenon have also been discovered. A previous study reported that non-alcoholic fatty liver (NAFLD) patients had decreased urea synthesis, so the team then compared the genetic changes in NAFLD mice with glucagon receptor knockout mice. Surprisingly, it turns out that both genes involved in amino acid metabolism are similarly down-regulated. Further studies have also shown that the appearance of fatty liver will damage the amino acid metabolism and urea production regulated by glucagon in mice. The analysis of clinical samples also confirmed the results of animal experiments: the plasma levels of glucagon and amino acids in NAFLD patients are higher. The researchers attributed this to decreased hepatic glucagon sensitivity in NAFLD patients.

　　The corresponding author of this article, Dr. Nicolai J. Wewer Albrechtsen of the Novoordisk Protein Research Center further explained: "Through the feedback system between the liver and pancreas, reduced glucagon sensitivity will increase the secretion of glucagon. Excessive levels of glucagon will promote sugar production in the liver, thereby increasing blood sugar levels." Insulin resistance has been found to be a common phenomenon in type 2 diabetes. In type 2 diabetes patients, prolonged hyperglycemia can cause pancreatic beta cells to produce more insulin and lower blood sugar levels. When the cells expressing insulin receptors in the human body are exposed to high levels of insulin for a long time, these cells will gradually become resistant to insulin and can no longer effectively control blood sugar.

　　In this study, the research team introduced a new concept, which is the opposite of "glucagon resistance" and "insulin resistance". "Glucagon resistance" caused by fatty liver may also be one of the causes of type 2 diabetes. Use a combination of glucagon and certain amino acids (such as alanine) controlled by the liver and pancreas feedback system as a marker. Fat content and glucagon inhibition can prevent and treat type 2 diabetes. Further research on the relationship between the concept of "glucagon resistance" and diabetes may help humans respond well to the threat of diabetes.