OBJECTIVE: Chemerin and vaspin are new adipokines which may modulate inflammatory response and insulin sensitivity in non-alcoholic fatty liver disease (NAFLD). The aims of this study were to assess: (1) circulating levels of chemerin and vaspin and their association with liver histology and markers of liver injury in NAFLD patients; and (2) the relationship between the analyzed adipokines and insulin resistance. MATERIAL AND METHODS: A total of 41 NAFLD patients with body mass index (BMI) 30.4 +/- 3.3 kg/m(2) [20 with non-alcoholic steatohepatitis (NASH) and BMI 30.3 +/- 3.3 kg/m(2) and 21 with simple steatosis/uncertain NASH (SS/UN) and BMI 30.5 +/- 3.4 kg/m(2)] and 10 healthy volunteers with BMI 24.0 +/- 2.9 kg/m(2) were included in the study. RESULTS: Serum chemerin concentration was significantly higher in NAFLD patients compared to healthy volunteers (p = 0.009). Serum chemerin was significantly higher in patients with NASH compared to patients with SS/UN (p = 0.009). The homeostasis model assessment for insulin resistance (HOMA-IR) value was higher in patients with NASH than in patients with SS/UN (p = 0.01). Serum chemerin and HOMA-IR were positively associated with NAFLD activity score (r = 0.40, p = 0.02; and r = 0.43, p = 0.008, respectively). Serum chemerin was associated with hepatocyte ballooning degeneration (r = 0.37; p = 0.03), total cholesterol (r = 0.45; p = 0.008) and diastolic blood pressure (r = 0.41; p = 0.02). HOMA-IR was related to fibrosis stage (r = 0.51; p = 0.001) and inflammatory activity grade in portal tracts (r = 0.40; p = 0.01). Serum vaspin correlated with hepatocyte ballooning degeneration (r = 0.31; p = 0.04), alanine aminotransferase and aspartate aminotransferase (r = 0.33, p = 0.03; and r = 0.32, p = 0.04, respectively) and diastolic blood pressure (r = 0.39, p = 0.01). CONCLUSIONS: This study shows for the first time that chemerin and vaspin serum concentrations are altered in patients with NAFLD. The analyzed adipokines appear to play a pivotal role in the pathogenesis of NAFLD, not only as regulators of insulin sensitivity, but also as mediators of the inflammatory process.
OBJECTIVE:Chemerin and vaspin are new adipokines which may modulate inflammatory response and insulin sensitivity in non-alcoholic fatty liver disease (NAFLD). The aims of this study were to assess: (1) circulating levels of chemerin and vaspin and their association with liver histology and markers of liver injury in NAFLD patients; and (2) the relationship between the analyzed adipokines and insulin resistance. MATERIAL AND METHODS: A total of 41 NAFLD patients with body mass index (BMI) 30.4 +/- 3.3 kg/m(2) [20 with non-alcoholic steatohepatitis (NASH) and BMI 30.3 +/- 3.3 kg/m(2) and 21 with simple steatosis/uncertain NASH (SS/UN) and BMI 30.5 +/- 3.4 kg/m(2)] and 10 healthy volunteers with BMI 24.0 +/- 2.9 kg/m(2) were included in the study. RESULTS: Serum chemerin concentration was significantly higher in NAFLD patients compared to healthy volunteers (p = 0.009). Serum chemerin was significantly higher in patients with NASH compared to patients with SS/UN (p = 0.009). The homeostasis model assessment for insulin resistance (HOMA-IR) value was higher in patients with NASH than in patients with SS/UN (p = 0.01). Serum chemerin and HOMA-IR were positively associated with NAFLD activity score (r = 0.40, p = 0.02; and r = 0.43, p = 0.008, respectively). Serum chemerin was associated with hepatocyte ballooning degeneration (r = 0.37; p = 0.03), total cholesterol (r = 0.45; p = 0.008) and diastolic blood pressure (r = 0.41; p = 0.02). HOMA-IR was related to fibrosis stage (r = 0.51; p = 0.001) and inflammatory activity grade in portal tracts (r = 0.40; p = 0.01). Serum vaspin correlated with hepatocyte ballooning degeneration (r = 0.31; p = 0.04), alanine aminotransferase and aspartate aminotransferase (r = 0.33, p = 0.03; and r = 0.32, p = 0.04, respectively) and diastolic blood pressure (r = 0.39, p = 0.01). CONCLUSIONS: This study shows for the first time that chemerin and vaspin serum concentrations are altered in patients with NAFLD. The analyzed adipokines appear to play a pivotal role in the pathogenesis of NAFLD, not only as regulators of insulin sensitivity, but also as mediators of the inflammatory process.
Authors: Stephanie W Watts; Emma S Darios; Adam E Mullick; Hannah Garver; Thomas L Saunders; Elizabeth D Hughes; Wanda E Filipiak; Michael G Zeidler; Nichole McMullen; Christopher J Sinal; Ramya K Kumar; David J Ferland; Gregory D Fink Journal: FASEB J Date: 2018-06-15 Impact factor: 5.191
Authors: Stephanie W Watts; Anne M Dorrance; Mark E Penfold; Jillian L Rourke; Christopher J Sinal; Bridget Seitz; Timothy J Sullivan; Trevor T Charvat; Janice M Thompson; Robert Burnett; Gregory D Fink Journal: Arterioscler Thromb Vasc Biol Date: 2013-04-04 Impact factor: 8.311
Authors: David J Ferland; Emma D Flood; Hannah Garver; Steve T Yeh; Stanley Riney; Adam E Mullick; Gregory D Fink; Stephanie W Watts Journal: Physiol Genomics Date: 2019-10-07 Impact factor: 3.107