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The relevance of this study lies in the lack of reliable information on the key aspects of the molecular mechanisms of fatty hepatosis, a common mammalian disease, and its dangerous complications, such as fibrosis, cirrhosis, and hepatocellular carcinoma. These circumstances substantially complicate the prompt diagnosis of this hepatopathology and reduce the effectiveness of treatment. The metabolism of the heme derivative bilirubin is unique and inherent in the liver, which undergoes transformation due to hepatocyte enzyme systems to form neutral compounds, such as glucurono-conjugates and sulphoconjugates, which undergoes changes and requires analysis in fatty hepatosis in animals. The aim of the study was to determine the characteristic changes in the content of unconjugated bilirubin and its sulphoconjugate, glucuronide, monoglucuronide, monoglucoside, and diglucuronide in the blood, bile, and liver of rats under the modelling of fatty hepatosis and the administration of rehabilitation therapy. For this, the thin-layer chromatography method was used. It was found that under tetracycline-induced fatty hepatosis in laboratory rats, the concentration of unconjugated bilirubin in the blood decreased by 39.3%, bilirubin glucuronide by 44.4%, and the total fraction of bilirubin monoglucuronide and monoglycoside by 78.9%. Oral administration of the milk phospholipid complex in the composition of the BAS “FLP-MD” to sick animals ensured the maintenance of these indicators at the control level. The content of bilirubin glucuronide and bilirubin diglucuronide decreased in the liver tissue of the treated rats. When these animals were administered a phospholipid-containing bioadditives, the level of unconjugated bilirubin in the liver tissue increased by 22.2%, but the content of its conjugated forms decreased. The content of all the studied bilirubin fractions decreased in the bile of sick rats during self-rehabilitation. The components of the BAS “FLP-MD” in fatty hepatosis in rats did not affect the reduction of unconjugated bilirubin in bile but eliminated the inhibitory effect of the modelled pathology on the content of all conjugated forms of bilirubin. The findings can be used as biochemical markers to monitor the pigment metabolism in the development of fatty hepatosis in mammals
Illek et al. (Tue,) studied this question.