One of the reasons of mortality associated with diabetes mellitus (DM) type 2 is liver disease. Nonalcoholic fatty liver disease (NFLD) includes: fatty dystrophy, nonalcoholic steatohepatitis and fibrosis with the possible transition to cirrhosis. Adipose tissue produces hormones – leptin and resistin. The question regarding the role and possible influence of these hormones in hyperinsulinemia, insulin resistance and atherogenesis of NFLD development still remains open.

The study involved 55 patients with type 2 diabetes and NFLD. Patients were divided into two groups: 1st – with no obesity (BMI < 29,9 kg / m2, n = 21); 2nd – with obesity presence (BMI > 30,0 kg/m2, n = 34). The level of leptin, resistin, insulin, NEFA and biochemical parameters were measured and compared in the patients. The experimental groups were comparable in age and compensation of diabetes. Significantly higher levels of leptin and insulin were found in the patients of the second experimental group, though considerable changes in the content of resistin and NEFA in the same group of the patients were not found.

The patients with obesity display hyperinsulinemia, due to which withdrawal of NEFA from the liver is suppressed. An accumulation of NEFA in the liver leads to damage of biological membranes of hepatocytes. Leptin directly affects the production of insulin, in addition, the resistance of the tissues to leptin can eventually develop with time, which promotes the growth of adipose tissue and slows or stops NEFA utilization in the liver. This suggests leptin possible pathogenetic factor in the development of NFLD.

It is believed that resistin level affects glucose and NEFA and reduces insulin sensitivity. The combination of these factors should cause insulin resistance, but the results of this research question remains controversial. Mechanism that causes the development of insulin resistance under the influence of hyperresistinaemia is still need to be found. Numerous studies conducted on mice indicate that resistin induces hepatic and peripheral insulin resistance. Our results did not reveal difference in the contents of resistin in patients with NFLD and type 2 diabetes based on the presence of obesity. Today there are many differences in the results of animals studies and studies in humans. Unlike animals, human fat cells produce significantly less resistin, which is only 64 % homologous to mice resistin, which complicates its definition. Based on our data, we can conclude that further research is necessary, but we may also suggest that elevated levels of blood resistin can be a trigger factor of metabolic disorders in type 2 diabetes regardless of whether obesity present or not.

The levels of ALT were different in two experimental group: 18,58 ± 1,94 IU/L υ 31,51 ± 5,13 IU/L, p = 0,04; indicating that damage and necrosis of hepatocytes, development of cytolysis syndrome in patients with NFLD and type 2 diabetes with obesity is more pronounced.

Therefore, the obtained results indicate that the significantly higher insulin and leptin levels were found in the patients with NFLD and type 2 diabetes with obesity. Pathogenetic role of resistin as the mechanism of NFLD with type 2 diabetes should be scrutinized. Imbalance of adipose tissue hormones is more pronounced in patients with NFLD and type 2 diabetes with obesity, metabolic disorders that affect liver function are activated and enhanced more evidently in type 2 diabetes with obesity respectively.

Keywords: diabetes mellitus type 2, nonalcoholic fatty liver disease, obesity, leptin, resistin

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