Related Mechanisms of RBP4 in Glycolipid Metabolism

Overview

Retinol binding protein 4 ( RBP4 ) is a newly discovered adipokine secreted by adipose tissue, which leads to insulin resistance ( IR ) and participates in the occurrence of T2DM. At present, it's not clear whether RBP4 can cause islet β cell dysfunction. The purpose of this study is to explore the role of serum apo-RBP4 in the pathogenesis of newly diagnosed T2DM patients.

In recent years, with the improvement of living standards and lifestyle changes, the incidence of type II diabetes is increasing, and T2DM has become a worldwide disease that seriously endangers people ' s health. When patients with diabetes in the middle and late, the condition is often irreversible, and early if effective treatment, help to improve the condition in a timely manner, delay the development of the disease process. Therefore, early diagnosis and treatment is the key to prevention and treatment of diabetes. Years of studies have shown that insulin resistance and β-cell dysfunction are the two major mechanisms of type II diabetes. Previous studies on the pathogenesis of type II diabetes mostly focused on insulin resistance, and there are few studies on β-cell dysfunction. Therefore, the study of islet β-cell dysfunction is extremely important. According to previous studies, the investigator found that although insulin resistance exists in type II diabetes, also exists to the same extent in many people who do not have diabetes. These people may have or do not have metabolic syndrome. Therefore, insulin resistance alone cannot be the decisive pathogenic factor of type II diabetes, and the increasing facts indicate that the abnormality of islet cells, especially islet β cells, may be the central link in the pathogenesis of type II diabetes. Obviously, insulin resistance is the initiating factor of type II diabetes, and the normal function of islet β cells is the determinant of whether type II diabetes occurs : the occurrence of insulin resistance initiates the pathogenesis of type II diabetes, but if the islet β cells can maintain its compensatory ability, type II diabetes will not occur. Once its compensatory ability decreases, type II diabetes gradually occurs. Therefore, islet β cell dysfunction is the key to the pathogenesis of type II diabetes. Exploring the harmful factors that impair β-cell function is critical for early prevention and treatment of diabetes.

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