The combination of hypertension, obesity and non-alcoholic fatty liver disease occurs in medical practice very often. A number of studies have shown that non-alcoholic fatty liver disease increases the risk of cardiovascular disease independently of other predictors and manifestations of the metabolic syndrome. Current issues of research and identification of common pathogenic relationships of obesity, hypertension, and liver steatosis are investigated in the article. According to the analysed literature, it is indicated that insulin resistance and compensatory hyperinsulinaemia are considered as one of the key factors in the development of this comorbidity. The processes of chronic inflammation are increasing with the growth of adipose tissue volume. Some researchers believe that non-specific systemic inflammation combines arterial hypertension, increased body weight (especially abdominal obesity), steatosis, dyslipidaemia, atherogenesis and arteriosclerosis into a single syndrome. The role of non-alcoholic fatty liver disease in the growth of the thickness of the intima-media complex was studied. It is known that adipose tissue functions as an endocrine organ, expresses genes encoding bioactive substances, and secretes certain cytokines. A strong link between dysfunction of adipose tissue in patients with non-alcoholic fatty liver disease and in such conditions as metabolic syndrome and cardiovascular disease was demonstrated. The dysfunction of the endothelium is also advisable to consider as the connecting link between liver disease, obesity and hypertension. Despite some understanding of common pathogenic mechanisms for the development of non-alcoholic fatty liver disease and hypertension, this comorbid pathology remains the subject of much debate and a variety of studies. key words: arterial hypertension, obesity, non-alcoholic fatty liver disease, insulin resistance, dyslipidaemia, non-specific systemic inflammation, endothelial dysfunction, atherogenesis.