LNK in Polycystic Ovary Syndrome With Insulin Resistance

Insulin Resistance Clinical Trial

Official title:

LNK Participates in Insulin Resistance in Polycystic Ovary Syndrome by Regulating Adipose Glucose Transport

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT05146063
• Other study ID #: SYSEC-KY-KS-2021-187
• Status: Recruiting
• Start date: November 5, 2021
• Est. completion date: December 31, 2023

Study information

• Verified date: November 2021
• Source: Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University
• Contact: Yi Zhang
• Phone: +862081332120
• Email: sys_iit[@]163.com
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

Insulin resistance (IR) is an important pathological feature of polycystic ovary syndrome (PCOS), with an incidence rate of up to 85%, which seriously affects the patient's fertility, quality of life, and offspring health, but the mechanism is unknown. The adaptor protein LNK is closely related to metabolic diseases. Our exome sequencing has found that the mutation rate of LNK gene in patients with PCOS and IR is high. Studies have found that LNK can affect adipose inflammation and impair glucose tolerance. Whether LNK is related to fat metabolism is worth further study. Our previous research found that: LNK expression was significantly increased in adipose tissue of patients with PCOS and IR. Knockout of LNK in PCOS IR model mice can reduce serum triglycerides, free fatty acids, high-sensitivity C-reactive protein levels and reduce fatty liver occurrence, which indicates that LNK has a mitigating effect on IR. Mechanism studies have shown that LNK knockout can upregulate the glucose transporter Glut4, also LNK and insulin receptor substrate IRS-1 can form protein complexes. Based on the above research basis, we propose the following scientific hypothesis: LNK in adipose tissue can regulate insulin signaling pathway by binding to IRS-1, downregulate Glut4, and participate in PCOS IR occurrence. This project intends to clarify the specific mechanism by which LNK regulates glucose transport and participate in IR in combination with clinical specimens, animal models and cell experiments, and provide scientific basis for LNK as a potential therapeutic target for PCOS IR.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 80
• Est. completion date: December 31, 2023
• Est. primary completion date: December 31, 2022
• Accepts healthy volunteers: No
• Gender: Female
• Age group: 18 Years to 40 Years

Eligibility

Inclusion Criteria:

• Patients with polycystic ovary syndrome who meet the 2003 Rotterdam criteria

Exclusion Criteria:

• Do not meet the diagnostic criteria for polycystic ovary syndrome

Related Conditions & MeSH terms

• Insulin Resistance
• Polycystic Ovarian Syndrome
• Polycystic Ovary Syndrome
• Syndrome

Intervention

Diagnostic Test:
• Take the patient's subcutaneous fat tissue to detect the expression of LNK
Take the patient's subcutaneous fat tissue to detect the mRNA and protein expression levels of LNK by RT-qPCR and western blot.

Locations

Country	Name	City	State
China	Sun Yat-sen Memorial Hospital, Sun Yat-sen University	Guangzhou	Guangdong

Sponsors (1)

Lead Sponsor	Collaborator
Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University

Country where clinical trial is conducted

China, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	mRNA expression levels of LNK	The expression level of LNK mRNA in the subcutaneous adipose tissue of the PCOS patients	2 years
Primary	protein expression levels of LNK	The expression level of LNK protein in the subcutaneous adipose tissue of the PCOS patients	2 years