Selenoprotein P and Non-alcoholic Fatty Liver Disease

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.

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Key information

Conditions

Non-Alcoholic Fatty Liver Disease Digestive System Diseases Fatty Liver Glucose Metabolism Disorders Hyperinsulinism Insulin Resistance Liver Diseases Metabolic Diseases Nutritional and Metabolic Diseases

Age range

20 year–80 year

Sex eligibility

All sexes

Study type

Observational

Primary location

Hae Yoon Choi

Seoul, 152-703, South Korea

About this study

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.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

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

Treatment and study plan

Primary outcomes

Association between SeP and NAFLD

Time frame: through study completion, an average of 2 year

We used multiple logistic regression analysis

Secondary outcomes

Compare SeP level between control and NAFLD group

Time frame: through study completion, an average of 2 year

using Mann-Whitney U test
Correlation between SeP level and cardiometabolic risk factors

Time frame: through study completion, an average of 2 year

SeP level was stratified by tertile.

Sponsors and collaborators

Lead sponsor

Korea University

Other

Registry information

Important dates

Study start: 2007
Primary completion: 2008
Study completion: 2008
First posted: Dec 10, 2010
Registry last updated: Sep 3, 2020

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Published trials that share one or more normalized conditions with this study.

Completed