Factors affecting serum levels of adipokines in Korean male patients with nonalcoholic fatty liver disease.
- Author:
Se Yong OH
1
;
Yong Kyun CHO
;
Tae Woo YOO
;
Jung Ho PARK
;
Hong Joo KIM
;
Dong Il PARK
;
Chong Il SOHN
;
Woo Kyu JEON
;
Byung Ik KIM
;
Chan Hee JUNG
;
Eun Jung RHEE
;
Won Young LEE
;
Sun Woo KIM
;
Ki Won OH
;
Eun Joo YUN
;
Eun Sook OH
Author Information
1. Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. choyk2004.cho@samsung.com
- Publication Type:Original Article
- Keywords:
Fatty liver;
Leptin;
Adiponectin;
Resistin
- MeSH:
Adipokines*;
Adiponectin;
Dyslipidemias;
Fasting;
Fatty Liver*;
Humans;
Insulin Resistance;
Leptin;
Liver;
Male*;
Obesity;
Resistin
- From:Korean Journal of Medicine
2006;71(1):58-66
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Adipokines are associated with various metabolic disorders including insulin resistance, obesity and dyslipidemia. Metabolic disorders have also been reported to be associated with nonalcoholic fatty liver disease (NAFLD). We aimed to estimate changes in serum adipokines levels according to the degrees of steatosis and to determine independent factors influencing serum adipokines levels in Korean male patients with NAFLD. METHODS: 65 Korean male patients were subjected. The degrees of steatosis were stratified into the three groups, Group I: normal liver (27 subjects), Group II: mild fatty liver (24 subjects) and Group III: moderate to severe fatty liver (14 subjects), according to ultrasonographic liver findings. The anthropometric parameters, fasting serum adipokine levels including leptin, adiponectin and resistin were measured in all subjects. The level of insulin resistance was estimated using the HOMA-IR. RESULTS: Serum leptin levels were significantly different among the three groups (mean+/-SD: Group I (2.052+/-1.071), Group II (2.879+/-1.016), Group III (4.457+/-1.965 ng/mL), p<0.001). Serum adiponectin and resistin levels were not significantly different among the three groups (p=0.184, p=0.649, respectively). BMI and HOMA-IR were independent factors of changes in serum leptin levels (p=0.026, p=0.001, respectively), but independent factors of changes in serum adiponectin and resistin levels were not observed. CONCLUSIONS: Our study support a indirect role to induce metabolic disorder for leptin in the pathogenesis of NAFLD, but do not support roles for adiponectin and resistin in the pathogenesis of NAFLD. BMI and HOMA-IR were only independent factors of changes in serum leptin levels.
