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.

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The prevalence of the BRAF(V600E)mutation increased significantly in PTCs diagnosed in the authors' institution. Improved detection and several causative factors, most likely environmental and changes in iodine intake, may contribute to the increasing occurrence of TC.

BackgroundA mass of visceral adipose tissue is one of the most important determinants of progressive liver injury in nonalcoholic fatty liver disease (NAFLD). In accordance, nonalcoholic steatohepatitis (NASH) and fibrosis are believed to occur more commonly in morbidly obese patients compared with nonobese NAFLD patients.Aim of the studyComparative analysis of NAFLD histopathologic features and angiogenesis activity in morbidly obese and nonobese subjects.Materials and methodsBiopsy samples from 40 severely obese (BMI ≥40 kg m−2) and 30 nonobese (BMI ≤30 kg m−2) NAFLD patients were examined. Kleiner’s classification was used to diagnose NASH by grading steatosis, cytoplasmatic ballooning of hepatocytes, and lobular inflammation. The severity of fibrosis was evaluated according to the liver fibrosis staging system. Qualitative and quantitative immunohistochemical analyses of VEGF A, Flk-1, and CD34 were performed to study angiogenesis and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method was used to study hepatocyte apoptosis.ResultsSeverely obese patients did not differ from nonobese patients with respect to age and sex distribution. NASH was diagnosed in nine (22.5%) severely obese patients and in seven (23.3%) nonobese patients. Fibrosis was more common in morbidly obese patients (82.5 vs. 43.5%, χ² = 11.71, p = 0.003) and was not associated with NASH. Moreover, the severity of fibrosis was greater in obese patients, as advanced fibrosis (bridging fibrosis and cirrhosis) occurred in six (15%) severely obese patients and in two (6.7%) nonobese patients. In morbidly obese individuals, angiogenesis was independent of NASH and was activated at the stage of simple steatosis. In severe obesity, there was a positive relationship between the stage of fibrosis and angiogenic activity.ConclusionIn severely obese patients, fibrosis is probably promoted by mechanisms independent of NASH. In these patients, angiogenesis is activated early in the natural history of NAFLD and correlates with the severity of fibrosis.

The aim of this study was to investigate hepatic chemerin mRNA, serum chemerin concentration, and immunohistochemical staining for chemerin and and chemokine receptor-like 1 (CMKLR1) in hepatic tissue in 56 morbidly obese women with nonalcoholic fatty liver disease (NAFLD) and to search for a relationship with metabolic and histopathological features. Chemerin mRNA was assessed by quantitative real-time PCR, chemerin, and CMKLR1 immunohistochemical expression with specific antibodies, while serum chemerin concentration was assessed with commercially available enzyme-linked immunosorbent assays. Serum chemerin concentration reached 874.1 ±234.6 ng/ml. There was no difference in serum chemerin levels between patients with BMI < 40 kg/m 2 and ≥ 40 kg/m 2 . Serum chemerin concentration tended to be higher in patients with hepatocyte ballooning, greater extent of steatosis, and definite nonalcoholic steatohepatitis (NASH). Liver chemerin mRNA was observed in all included patients and was markedly, but insignificantly, higher in those with BMI ≥ 40 kg/ m 2 , hepatocyte ballooning, greater extent of steatosis, and definite NASH. Hepatic chemerin mRNA might be a predictor of hepatic steatosis, hepatocyte ballooning, and NAFLD activity score (NAS) but seemed not to be a primary driver regulating liver necroinflammatory activity and fibrosis. The lack of association between serum chemerin and hepatic chemerin mRNA may suggest that adipose tissue but not the liver is the main source of chemerin in morbidly obese women.