Selenoprotein P and Non-alcoholic Fatty Liver Disease

Insulin Resistance Clinical Trial

Official title:

Selenoprotein P and Non-alcoholic Fatty Liver Disease

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01257685
• Other study ID #: SEPP1(NAFLD)
• Status: Completed
• Start date: September 2007
• Est. completion date: August 2008

Study information

• Verified date: August 2020
• Source: Korea University
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

The pathogenesis of nonalcoholic fatty liver disease has not been fully elucidated. The most widely supported theory implicates insulin resistance as the key mechanism leading to hepatic steatosis, and perhaps also to steatohepatitis.

Selenoprotein P(SeP) is a secretory protein primarily produced by the liver. Previous studies demonstrated that SeP, a liver-derived secretory protein, causes insulin resistance.

Therefore, the purpose of this study is to determine the different Sep levels between healthy normal group and NAFLD group.

Description:

Nonalcoholic fatty liver disease (NAFLD), a disease spectrum that includes simple steatosis, nonalcoholic steatohepatitis (NASH) and cirrhosis, has been increasingly recognized as the hepatic manifestation of metabolic syndrome. Both inflammation and insulin resistance are considered to be pivotal pathogenic mechanisms of NAFLD, as well as metabolic syndrome, type 2 diabetes, and atherosclerosis. There is mounting evidence implicating adipokines secreted from adipose tissue in the pathogenesis and progression of NAFLD, in addition to the development of insulin resistance and inflammation. Selenoprotein P (SeP) has recently been reported as a novel hepatokine that regulates insulin resistance and systemic energy metabolism in rodents and humans. Although previous studies have shown a close relationship among insulin resistance, inflammation, and NAFLD, as far as we know, there is no previous report evaluating the association between SeP and NAFLD. In the present study, we examined serum SeP levels in subjects with increased visceral fat area (VFA) or liver fat accumulation measured with computed tomography (CT). We evaluated the relationship between SeP levels and cardiometabolic risk factors.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 120
• Est. completion date: August 2008
• Est. primary completion date: August 2008
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 20 Years to 80 Years

Eligibility

Inclusion Criteria:

• Healthy volunteers for visiting routine medical check in our clinic

Exclusion Criteria:

• History of cardiovascular disease(myocardial infarction, unstable angina, or cardiovascular revascularization)

• Diabetes

• Hypertension

• Malignancy

• Severe renal or hepatic disease

• Subjects taking medications that might affect body weight or body composition

Related Conditions & MeSH terms

• Fatty Liver
• Insulin Resistance
• Liver Diseases
• Non-alcoholic Fatty Liver Disease

Locations

Country	Name	City	State
Korea, Republic of	Hae Yoon Choi	Seoul

Sponsors (1)

Lead Sponsor	Collaborator
Korea University

Country where clinical trial is conducted

Korea, Republic of, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Association between SeP and NAFLD	We used multiple logistic regression analysis	through study completion, an average of 2 year
Secondary	Compare SeP level between control and NAFLD group	using Mann-Whitney U test	through study completion, an average of 2 year
Secondary	Correlation between SeP level and cardiometabolic risk factors	SeP level was stratified by tertile.	through study completion, an average of 2 year