Related Mechanisms of RBP4 in Glycolipid Metabolism

Not Applicable

Completed

• Conditions: Beta Cell Dysfunction
• Interventions: Biological: overexpression STRA6/miRNA3

• Registration Number: NCT05576168
• Lead Sponsor: Shanghai 10th People's Hospital

Brief 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.

Study Timeline

• Study Start: 2018-05-01
• Primary Completion: 2020-06-01
• Study Completion: 2021-07-01
• Study First Submitted: 2022-09-28
• Status Verified: 2022-10
• Study First Submitted QC: 2022-10-08
• Last Update Submitted: 2022-10-08
• Study First Posted: 2022-10-12
• Last Update Posted: 2022-10-12

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 200

Inclusion Criteria

1. Prior to conducting any trial-related activities, including those conducted to assess the subject's eligibility Informed consent of the subject;
2. Aged 18-60 years at the time of screening;
3. The diagnosis of diabetes was defined as fasting blood glucose above 7.0mmol/ L twice on different days on a normal diet

Exclusion Criteria

1. HIV, hepatitis B or C ( self-reported ) or active pulmonary tuberculosis history :
2. history of malignant tumor ;
3. Severe liver dysfunction or kidney disease ( AST or ALT > 3 times the normal upper limit, or eGFR < 30ml min 1.73 m2 ) ;
4. History of severe cardiovascular and cerebrovascular diseases ( angina pectoris, myocardial infarction or stroke ) in the past 6 months :
5. history of severe gastrointestinal disease or gastrointestinal surgery in the past 12 months ;
6. There are other diseases that affect glucose and lipid metabolism : hyperthyroidism, hypothyroidism, cortex Hyperalcoholism, etc. ;
7. Secondary diseases or drugs lead to obesity, including : elevated cortisol ( such as Cushing 's syndrome ), sagging Obesity caused by body and hypothalamus injury, obesity caused by weight loss drug reduction / discontinuation, etc.
8. Drugs affecting body weight or energy intake / energy expenditure were used within 3 months before screening, including :

Sex steroids ( intravenous, oral or intra-articular ), tricyclic antidepressants, for psychiatric disorders

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: PARALLEL

Arm && Interventions

Group	Intervention	Description
T2DM group	overexpression STRA6/miRNA3	patients with T2DM
control group	overexpression STRA6/miRNA3	patients without T2DM

Primary Outcome Measures

Name	Time	Method
RBP4	3 years	Retinol binding protein 4

Secondary Outcome Measures

Name	Time	Method
AST	3 years	aspartate aminotransferase in U/L
PBG	3 years	postprandial blood-glucose in mmol-L
PINS	3 years	postprandial serum insulin in mU/L
UA	3 years	Uric acid in umol/L
FT	3 years	free testosterone (nmol/L)
BMI	3 years	BMI=weight(kg)/heihgt(m)\^2
TT	3 years	total testosterone in mmol/L
FSH	3 years	follicle-stimulating hormone in IU/L
HOMA-IR	3 years	Homeostatic model assessment insulin resistance index=FBG\*FINS/22.5
FBG	3 years	fasting blood-glucose in mmol/L
FINS	3 years	fasting serum insulin in mU/L
ALT	3 years	alanine aminotransferase in U/L
TG	3 years	Triglyceride(mmol/L)
HDL-C	3 years	Hight-density lipoprotein cholesterol in mmol/L
TC	3 years	Total Cholesterol(mmol/L)
HbA1c(%)	3 years	Glycated hemoglobin
LDL-C	3 years	low-density lipoprotein cholesterol in mmol/L

Trial Locations

Locations (1)

Xiaoyun Cheng; 🇨🇳 Shanghai, Shanghai, China