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.
Keywords: alimentary stomatitis, high-fat diet, dysbiosis, antidisbiotic agent. Aim: тo investigate the prophylactic effect of the antidisbiotic phytopreparation kvertulin on the condition of the oral mucosa (OM) of rats with alimentary stomatitis. Methods. Alimentary stomatitis was reproduced in rats fed with 15% palm oil and with drinking water - lincomycin. After 40 days of feeding the rats, the activity of elastase, catalase, urease, lysozyme, and the content of malondialdehyde (MDA) were determined in the OM. The antioxidant-prooxidant index (API) was calculated from the ratio of catalase activity and MDA content, and the degree of dysbiosis was calculated from the ratio of relative urease and lysozyme activities. Results: In rats that consumed palm oil on the background of dysbiosis, the level of elastase, MDA, urease in OM significantly increased and the level of catalase and lysozyme decreased.The API index also decreases, but the degree of dysbiosis increases. In rats treated with palm oil on the background of dysbiosis and at the same time phytopreparation kvertulin, the levels of elastase, MDA, urease decreased in OM, but the level of catalase, lysozyme, API index significantly increased. The degree of dysbiosis was significantly reduced. Conclusion. Prevention of alimentary stomstitis by preparation kvertulin equal to 34 %.
More than 20 % of people over the age of 50 suffer from osteoporosis. Lipids play an important role in the pathogenesis of osteoporosis. Background. To investigate the effect of ordinary (high-linoleic) sunflower oil (OSO) on the state of periodontal bone tissue. Methods. In 5 series of experiments, determine the mineralization activity of the alveolar appendix of the mandible rats that were obtained with feed 5 or 15 percent of OSO for from 22 to 75 days. Mineralizing activity was determined by the ratio of activity of alkaline and acid phosphatase. In liver lipids (fractions of phospholipids and free fatty acids) were determined by the content of long-chain polyunsaturated fatty acids (LCPUFA) by the gas chromatographic method. Results. A decrease in mineralizing activity in OSO consumption, especially when using a feed with 15 % of OSO against a dysbiosis or metabolic syndrome. A significant (almost 10 times) is shown to reduce the content of ω-3 PUFA in fraction of phospholipids of the liver of rats receiving a diet with a content of OSO. Conclusion. Sunflower oil reduces the mineralizing activity of periodontal bone tissue by reducing the endogenous biosynthesis of ω-3 PUFA.
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".
Background. To determine the effect of antidysbiotic agent on the biosynthesis of fatty acids of lipids in the liver of rats fed a high-fat diet (HFD) with palm oil against the background of dysbiosis. Methods. The HFD contained 15% palm oil. In a biological experiment, white rats were used, divided into 4 groups: the 1st group received a fat-free diet (FFD), the 2nd, 3rd, and 4th received HFD. In rats of the 3rd and 4th groups, dysbiosis was reproduced using lincomycin. Rats of the 4th group from the first day of the experiment received an antidysbiotic agent (inulin + quercetin, ADA) with food. The duration of feeding is 39 days. Liver lipids were divided into 3 fractions: neutral lipids (NL), phospholipids (PL), and free fatty acids (FFA). The fatty acid composition of the fractions was determined by gas chromatography. The “activities” of fatty acid synthase, palmitic acid elongase, and stearyl-CoA- desaturase (SCD18 and SCD16) were determined. Results. The presence of all classes of fatty acids (FA) in the liver lipids of rats treated with FFD was established. Consumption of HFD with palm oil increased the content of NL in the liver by 6 times (gr. 2), and in group 3 by 8 times. The introduction of ADA reduces the content of NL almost to the level of the 1st group. The content of ω-3 polyunsaturated fatty acids (PUFA) decreases in the PL fraction in rats of the 3rd group and is restored in rats of the 4th group. In rats treated with HFD, the "activity" of synthase, SCD18 and very strongly SCD16 are reduced. Conclusion: The negative effect of palm oil on the background of dysbiosis on the biosynthesis of fatty acids in the liver, leading to hepatic steatosis and deficiency of ω-3 PUFA, can be prevented by the use of an antidysbiotic agent.
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