Background. Desaturase enzymes are involved in the formation of monoenoic acids from saturated fatty acids. One such enzyme is stearyl-CoA-desaturase (SCD1), which converts stearic acid to oleic acid. The aim of this work was to determine the effect of edible fats with different fatty acid compositions on SCD1 activity. Methods. High linoleic sunflower oil (HLSO), high oleic sunflower oil (HOSO) and palm oil (PO) were used. The rats were fed for 30 days with a semi-synthetic diet that did not contain any fats (FFD) and fat diets containing 5 % of each of the above oils. In animals, lipids were extracted from serum and liver and divided into 3 fractions: neutral lipids (NL), phospholipids (PL), and free fatty acids (FFA). The fatty acid composition of each fraction was determined by gas chromatography. The SCD18 activity was determined by the C18:1 n-9/C18:0  ‒ ratio, and the SCD16 activity was determined by the C16:1 n-7/C16:0  ratio. Results. A higher activity of SCD16 and SCD18 was found in the NL fraction, and the activity of SCD18 significantly exceeds that of SCD16. A decrease in the content of C16:0, C16:1 and C18:0 in the NL fraction of the liver and blood serum was shown. The activity of SCD16 in blood serum and liver decreases in rats fed fat diets­, while the activity of SCD18 does not decrease, and even increases with the consumption of HOSO.­ Conclusions. To determine the SCD1 activity, it is advisable to use the C18:1/C18:0 ratio in terms of the level of fatty acids in the NL fraction. Fatty diet inhibits SCD16 activity, and consumption of HOSO increases SCD18 activity.

Aim. To determine the main factors of inadequate fat diet (IAFD) and indicate the ways of their change. Methods. Analysis and generalization of existing scientific literature data and the results of our own research. Results. The following factors of IAFD have been identified: 1) excess fat in the diet; 2) an excess of palmitic acid in dietary fats; 3) an excess of linoleic acid in dietary fats; 4) consumption of thermoperoxide fats; 5) deficiency of ω-3 polyunsaturated fatty acids (PUFA). Conclusion. IAFD is a cause of metabolic and neuropsychiatric disorders underlying non-communicable diseases.

Aim. It has been established that the consumption of thermoperoxide fats causes the development of pathological processes in the tissues of the mouth, stomach, intestines and liver. The purpose of this work is to determine the possibility of their normalization using oral applications of phytogels.Methods. Thermoperoxide oil (TPSO) was obtained by heating sunflower oil in the presence of H2O2 at a temperature of +180 °C for 60 minutes. Oral TPSO applications were made on the oral mucosa at a dose of 2.25 g/kg daily for 5 days. Used mucose-adhesive phytogels "Kvertulin" (quercetin + inulin), "Biotrit" (juice from wheat sprout) and "Dubovy" (extract of polyphenolic compounds from oak wood) in the form of oral applications at a dose of 2.25 g/kg for half an hour before TPSO applications daily for 5 days. Elastase and urease 82 activity and malonic dialdehyde (MDA) content were determined in homogenates of the mucous membranes of the cheek, stomach, small and large intestines, as well as in the liver.Results. Oral applications of TPSO increased the levels of MDA, elastase and urease in the tissues of the digestive system. Applications of phytogels significantly normalized these parameters.Conclusions. Oral applications of TPSO cause the development of inflammation in the digestive system, especially in the liver. Oral applications of phytogels have a protective effect, especially "Kvertulin".

Keywords: liver, dysbiosis, nutrition, fats, oleic acid, sunflower. Aim: To determine the pathogenic effect of dysbiosis on the condition of the liver, as well as to study the possibility of the therapeutic effect of pomace from seeds of high oleic sunflower. Methods: Used pomace from seeds of high-oleic sunflower (fat content 8.9%, oleic acid 84%), and as a comparison drug – mill cake from seeds of high-linoleic sunflower (fat content 9.1%, linoleic acid 54%). Dysbiosis was induced in rats with lincomycin.Oilcakes were added to the composition of the feed in the amount of 10%. Feeding lasted 18 days. In the liver homogenate, the level of markers of inflammation and dysbiosis: elastase, MDA and urease, as well as the activity of defense enzymes: catalase and lysozyme were determined.In the blood serum, the level of indicators of dysbiotic syndrome was determined: the activity of urease, elastase and ALT. The pathogenic effect of dysbiosis on the liver was calculated according to the degree of change in the level of markers, and their therapeutic effect was calculated according to the degree of change in the level of markers under the influence of pomace feeding. Results: The introduction of lincomycin causes an increase in the serum activity of urease, elastase and ALT. In the liver, the level of urease, elastase and MDA increases, but the activity of lysozyme and catalase decreases. Feeding with high oleic pomace normalizes indicators. Conclusions: Dysbiotic syndrome causes the development of hepatitis, which can be prevented by feeding with high oleic pomace.

Aim. To determine the effects on the body of high-fat diets (HFD) with different fatty acid composition.Methods. Used ordinary sunflower, olive, palm and butter, which were introduced into the feed in an amount of 15 %. Rats were fed for 41 days. Gum, liver, small intestinal mucosa were isolated and blood serum was obtained, which determined the activity of elastase, ALT and alkaline phosphatase, as well as the content of glucose, triglycerides and cholesterol. The activity of elastase, catalase, urease, lysozyme, and MDA content were determined in tissue homogenates. The API index and the degree of dysbiosis were calculated.Results. In rats treated with HFD, elastase, urease, MDA content increased, but lysozyme and catalase activity decreased in all tissues, the API index also decreased, and the degree of dysbiosis increased significantly. Serum triglycerides and cholesterol increased. Stronger pathological changes occurred in rats treated with palm or butter, and the lowest in rats treated with olive oil.Conclusion. HFD causes the development of dysbiosis, decreased levels of antioxidant protection and the development of inflammation, more pronounced with the consumption of fats high in palmitic acid.