Selenoprotein P and Non-alcoholic Fatty Liver Disease

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT01257685

Enrollment

120

Registered

2010-12-10

Start date

2007-09-30

Completion date

2008-08-31

Last updated

2020-09-03

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Insulin Resistance, Non-alcoholic Fatty Liver Disease

Brief 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.

Detailed 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.

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

CROSS_SECTIONAL

Eligibility

Sex/Gender

ALL

Age

20 Years to 80 Years

Healthy volunteers

Yes

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

Design outcomes

Primary

Measure	Time frame	Description
Association between SeP and NAFLD	through study completion, an average of 2 year	We used multiple logistic regression analysis

Secondary

Measure	Time frame	Description
Compare SeP level between control and NAFLD group	through study completion, an average of 2 year	using Mann-Whitney U test
Correlation between SeP level and cardiometabolic risk factors	through study completion, an average of 2 year	SeP level was stratified by tertile.

Countries

South Korea

Outcome results