Author details

All these mechanisms show how changes in the microbiota, in combination with loss of innate

Gut microbiota also influences bile acid metabolisms mainly through the stimulation of the bile-acid-activated nuclear receptor and also by interacting with farnesoid X receptor (FXR) which induce excretion of bile acids from the liver and production of antimicrobial peptides

Although significant progress has been made in NAFLD/NASH related HCC, many issues still remain to be resolved. With the prevalence of HCV declining in the last years, the incidence of NAFLD/NASH is expected to account for a greater proportion of HCC incidence in the near future due to the growing epidemic of obesity, diabetes and metabolic syndrome, known as independent metabolic risk factors for development of HCC. The annual incidence rate of HCC developed in patients with NASH-related cirrhosis is not yet clearly established and recent evidence show that a significant number of patients with NAFLD or NASH progress to HCC in the absence of hepatic cirrhosis. NAFLD/NASH-related cirrhotic patients receive significantly less surveillance for HCC than those with HCV-related cirrhosis, in contrast to epidemiological data and this represents an important public health problem. Also dysbiosis play an important role in progression of liver disease via changes in bile acids metabolism and

In conclusion, metabolic syndrome comprising of obesity, type 2 diabetes, dyslipidemia, hypertension, is related with an increased risk for development of HCC. NAFLD considered the liver manifestation of metabolic syndrome is an important factor implicated in progression to HCC. Also alteration in gut microbiota seems to be connected with HCC occurrence but

immune sensors, may induce metabolic liver disorders.

[65].

104 Liver Cancer

4. Conclusions

dysregulation of intestinal barrier.

Acknowledgements

Conflict of interest

many questions still remain to be answered.

All authors contributed equally to this chapter.

The authors declare no conflict of interest regarding this review.

Andra-Iulia Suceveanu1 \*, Laura Mazilu<sup>2</sup> , Andreea-Daniela Gheorghe<sup>2</sup> , Anca Pantea Stoian<sup>3</sup> , Felix Voinea<sup>4</sup> and Adrian-Paul Suceveanu5

\*Address all correspondence to: andrasuceveanu@yahoo.com

1 Faculty of Medicine, Department of Gastroenterology, Emergency Hospital of Constanta, Ovidius University, Constanta, Romania

2 Faculty of Medicine, Department of Oncology, Emergency Hospital of Constanta, Ovidius University, Constanta, Romania

3 University of Medicine and Farmacy, Carol Davila, Department of Diabetes, Nutrition and Metabolic Disease, Bucharest, Romania

4 Faculty of Medicine, Department of Urology, Emergency Hospital of Constanta, Ovidius University, Constanta, Romania

5 Faculty of Medicine, Department of Internal Medicine, Emergency Hospital of Constanta, Ovidius University, Constanta, Romania
