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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.
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.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Control Group | Normal group | ||
| NAFLD Group | NAFLD in the present study was defined a value of LAI <5 HU using an unenhaned CT. |
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| Measure | Description | Time Frame |
|---|---|---|
| Association between SeP and NAFLD | We used multiple logistic regression analysis | through study completion, an average of 2 year |
| Measure | Description | Time Frame |
|---|---|---|
| Compare SeP level between control and NAFLD group | using Mann-Whitney U test | through study completion, an average of 2 year |
| Correlation between SeP level and cardiometabolic risk factors | SeP level was stratified by tertile. |
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Inclusion Criteria:
Exclusion Criteria:
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Healthy volunteers for visiting routine medical check in our clinic
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| Name | Affiliation | Role |
|---|---|---|
| Kyung Mook Choi, MD.PhD | Korea University | Study Director |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Hae Yoon Choi | Seoul | 152-703 | South Korea |
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| ID | Term |
|---|---|
| D065626 | Non-alcoholic Fatty Liver Disease |
| D007333 | Insulin Resistance |
| ID | Term |
|---|---|
| D005234 | Fatty Liver |
| D008107 | Liver Diseases |
| D004066 | Digestive System Diseases |
| D006946 | Hyperinsulinism |
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blood samples. Abdominal VFA and total abdominal fat area were measured via CT scan without an intravenous contrast agent
| through study completion, an average of 2 year |
| D044882 |
| Glucose Metabolism Disorders |
| D008659 | Metabolic Diseases |
| D009750 | Nutritional and Metabolic Diseases |