Serum Adropin Levels Are Reduced in Adult Patients with Nonalcoholic Fatty Liver Disease.

OBJECTIVES: Adropin is a novel marker of metabolic syndrome and insulin resistance. The aim of this study was to explore the association of serum adropin levels with hepatosteatosis among adult patients. MATERIALS AND METHODS: Serum biochemical parameters including liver and renal function tests, insulin levels, and serum adropin levels were compared between adult patients with nonalcoholic fatty liver disease (NAFLD) and healthy control cases. RESULTS: A total of 51 patients with a mean age of 37.9 ± 9.96 years diagnosed with grade 2-3 hepatosteatosis and 30 healthy control cases with a mean age of 34.8 ± 9.5 years were included in the study. Serum adropin levels in the NAFLD group were statistically significantly lower than in the control cases (588.4 ± 261.0 vs. 894.2 ± 301.2, respectively; p < 0.001). The study participants were further subdivided into 2 groups as patients with (n = 35) or without (n = 46) insulin resistance using the serum homeostatic model of assessment-insulin resistance (HOMA-IR). Serum adropin levels were statistically significantly lower in patients with insulin resistance (p < 0.01). There was a negative correlation between adropin levels and serum insulin, HOMA-IR, urea, gamma-glutamyl transferase, total cholesterol, and triglyceride levels. CONCLUSION: We observed a decrease in serum adropin levels among adult patients with NAFLD. We also found lower levels of serum adropin in patients with insulin resistance, supporting previous data in the literature. Studies investigating the association of adropin levels with other inflammatory parameters are warranted to define its exact role in the pathogenesis of hepatosteatosis.

Serum Angiopoietin-like peptide 4 levels in patients with hepatic steatosis.

OBJECTIVES: Angiopoietin-like peptide 4 (ANGPTL-4) plays an important role in lipid metabolism by inhibiting the enzyme lipoprotein lipase. This effect of ANGPTL-4 results in suppression of the release of plasma triglyceride-derived fatty acids. Increase in fatty acid levels entering to the liver and abnormalities in their secretion is one of the main mechanisms in pathogenesis of hepatic steatosis. In this study, we aimed to investigate the role of ANGPTL-4 in pathogenesis of hepatic steatosis by determining its levels in patients with fatty liver disease. METHODS: Totally 51 patients (age: 37.9 ±â€¯9.9 years, M/F) diagnosed with grade 2-3 hepatic steatosis with ultrasound and 30 healthy volunteers (age: 34.8 ±â€¯9.5 years, M/F) were included in the study. In both groups, routine biochemical tests including fasting blood glucose, fasting insulin levels, triglyceride, total cholesterol, LDL- cholesterol, HDL-cholesterol, AST, ALT, ALP, GGT levels were measured together with the ANGPTL-4 levels. In determination of ANGPTL-4 levels, ELISA was performed. RESULTS: When compared with the control group, ANGPTL-4 levels were determined to be decreased in patients with hepatic steatosis (369 ±â€¯243 vs 303 ±â€¯286 ng/mL, p = 0.014). There was a negative weak correlation observed between ANGPTL-4 and triglyceride levels (r = -0.246, p = 0.027). Among all groups, when patients with and without insulin resistance were compared; ANGPTL-4 levels were determined to be similar. While fasting blood glucose levels were similar between 2 groups; fasting insulin and triglyceride levels were determined to be increased in hepatic steatosis group (Insulin 17.7 ±â€¯12 vs 7.4 ±â€¯3.3 µIU/mL, p < 0.001, triglyceride 158 ±â€¯46.4 vs 118 ±â€¯59.8 mg/dL p < 0.001). CONCLUSIONS: We have determined lower serum ANGPTL-4 levels in patients with hepatic steatosis. ANGPTL-4 that is regulating LPL activity plays an important role in fatty liver disease pathogenesis via free fatty acid metabolism and peroxisome proliferator-activated receptor-delta (PPAR-δ). We believe that the results of this study would elucidate the investigations about the mechanism of fatty liver disease development and treatments targeting ANGPTL-4.

The relationship between left ventricular mass and insulin resistance in obese patients.

OBJECTIVE: In this study, we investigated the relationship between left ventricular mass and insulin resistance in obese patients. METHODS: A total of 90 subjects, 66 women, and 24 men, with an age range from 24 to 56 years, were enrolled in the study. Forty-nine patients were in the obesity group whose body mass index (BMI) was >29.9kg/m(2) and 41 subjects were in the control group with a BMI <25kg/m(2). All of them were normotensive, nondiabetic, and did not have any cardiovascular disease. They were not taking any medication. Weight, height, and waist circumference were measured and BMI was calculated. Plasma glucose, insulin, serum total, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, and triglyceride levels were measured, and insulin resistance was calculated via homeostasis model of assessment-estimated insulin resistance (HOMA-IR). Subjects were examined by echocardiography and left ventricular mass (LVM) and index (LVMI) were calculated with Devereux formula. RESULTS: Insulin levels, HOMA-IR, LVM, and LVMI were significantly higher in obesity group (p<0.01). Fasting glucose, triglyceride, fasting insulin levels, and waist circumference did not correlate with LVMI. CONCLUSION: In conclusion, though findings of the present study suggest increased left ventricular hypertrophy (LVH) in obese subjects compared to controls, it appears that the increased LVM or LVH is not linked to BMI and insulin resistance in this study population.