Vaspin mRNA levels in the liver of morbidly obese women with nonalcoholic fatty liver disease.

The aim of this study was to evaluate hepatic vaspin mRNA in morbidly obese women with nonalcoholic fatty liver disease (NAFLD) and to look for its relationships with metabolic and histopathological features. The study included 56 severely obese women who underwent intraoperative wedge liver biopsy during bariatric surgery. Hepatic vaspin mRNA was assessed by quantitative real-time PCR. Vaspin mRNA found in all included patients was markedly higher in patients with body mass index (BMI) ≥ 40 kg/m2 (4.59 ±3.09 vs. 0.44 ±0.33; p = 0.05). An evident but statistically insignificant difference in vaspin mRNA levels was observed between patients with and without hepatocyte ballooning (4.77 ±4.23 vs. 0.45 ±0.29, respectively), with and without steatosis (4.80 ±4.20 vs. 0.41 ±0.29, respectively), without and with fibrosis (0.25 ±0.80 vs. 6.23 ±7.2, respectively), and those without and with lobular inflammation (0.27 ±1.0 vs. 5.55 ±10.1, respectively). There was marked difference in vaspin mRNA between patients with simple steatosis/borderline nonalcoholic steatohepatitis (NASH) compared to those with definite NASH (0.24 ±0.96 vs. 10.5 ±10.4). Adiposity is an undoubted confounding factor influencing vaspin levels. Hepatic vaspin mRNA seems to be markedly elevated in morbidly obese patients with more advanced NAFLD and when hallmarks of NASH were observed. Pointing to non-linear mRNA levels within the NAFLD spectrum and an evident increase in patients with fibrosis and definite NASH, the detrimental action of vaspin cannot be excluded.

From the stomach to other organs: Helicobacter pylori and the liver.

Many recent studies have examined the importance of Helicobacter pylori (H. pylori) infection in the pathogenesis of the diseases outside the stomach and explored the significance of this bacterium in the pathogenesis of some metabolic and cardiovascular diseases. Recent studies have provided evidence that H. pylori is also involved in the pathogenesis of some liver diseases. Many observations have proved that H. pylori infection is important in the development of insulin resistance, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver fibrosis and cirrhosis. The worsening of liver inflammation of different origins also occurs during H. pylori infection. Some studies have indicated that H. pylori infection induces autoimmunological diseases in the liver and biliary tract. The potential significance of this bacterium in carcinogenesis is unclear, but it is within the scope of interest of many studies. The proposed mechanisms through which H. pylori impacts the development of hepatobiliary diseases are complex and ambiguous. The importance of other Helicobacter species in the development of hepatobiliary diseases is also considered because they could lead to the development of inflammatory, fibrotic and necrotic injuries of the liver and, consequently, to hepatocellular carcinoma. However, many contrary viewpoints indicate that some evidence is not convincing, and further studies of the subject are needed. This review presents the current knowledge about the importance of H. pylori in the pathogenesis of liver and in biliary diseases.

Visfatin and TGF-Β1 in primary biliary cirrhosis and two other common liver diseases.

UNLABELLED: The aim of this study is to investigate plasma concentration of visfatin and transforming growth factor Β1 (TGF-Β1) in three groups of patients: primary biliary cirrhosis (PBC), non-alcoholic fatty liver disease (NAFLD) and toxic cirrhosis (TC). We qualified the patients into the study and assigned them to the appropriate group according to clinical examination, laboratory tests and ultrasound imaging technic (US). We showed that plasma concentrations of visfatin in PBC, NAFLD and TC group were respectively 1.41 ± 1.76 ng/mL, 1.22 ± 1.08 ng/mL and 0.70 ± 1.22 ng/mL. Plasma concentration of visfatin was significantly lower in TC group than in others both (p ± 0.017). The differences of visfatin concentration between NAFLD and TC group were not statistically significant. The values of TGF-Β1 in PBC, NAFLD and TC group were respectively 21031 ± 7822 pg/mL, 21588 ± 12639 pg/mL, and 9678 ± 4757 pg/mL. The statistical analysis showed that the value of cirrhotic group was significantly (p ±0.017) lower compared to both others groups. The difference between PBC and NAFLD was insignificant. IN CONCLUSION: Despite the PBC and NAFLD are the diseases of different pathogenesis and origin, plasma concentration of visfatin and TGF-Β1 were similar in these both groups but significantly lower in TC probably due to decreased activity as well as number of cells producing these cytokines in the cirrhotic liver.