Related Mechanisms of RBP4 in Glycolipid Metabolism
Condition: Beta Cell Dysfunction
Study type: Interventional

Summary: 
      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.
    

Detailed description: 
      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.
    

Intervention name(s): overexpression STRA6/miRNA3
Intervention type(s): Biological
Intervention description(s): RBP4 express in patients with T2DM or not
Other intervention name(s): RBP4 express in T2DM patients
Allocation: Non-Randomized
Intervention model: Parallel Assignment
Intervention model description: Serum RBP4 level in patients with or without type 2 diabetes
Masking: None (Open Label)
Primary purpose: Treatment
Keywords: Retinol binding protein 4; beta cell dysfunction; glycolipid metabolism