MORPHOFUNCTIONAL STATE OF THE LIVER IN RATS WITH FATTY HEPATOSIS MODELING AND ALTERED THYROID STATUS
Abstract
Introduction. The prevalence of thyroid pathology, along with the increasing incidence of hepatobiliary diseases, necessitates studying the influence of thyroid status on the “natural history” of liver disease development. Objective. To evaluate the morphofunctional state of the liver in rats with drug-induced hypo- and hyperthyroidism using a model of chronic fatty hepatosis. Materials and methods. Models of hyperthyroidism (I) and hypothyroidism (II) were reproduced. Animals in the experimental groups received 15 and 30% fructose solutions instead of drinking water. Decapitation was performed after 45 days. Liver fragments were fixed in 10% neutral formalin for 24 hours. Sections with a thickness of 3–4 μm were prepared and subjected to histological examination. Results. The vascularization index was highest in group I with a 15% fructose load. Liver sinusoids occupied the maximum area relative to the area of the liver tissue image. With a 30% fructose load against a background of hypo- and hyperthyroidism, the lumen of the sinusoids appeared narrowed. The relative content of connective tissue in the liver parenchyma of the experimental groups did not statistically significantly depend on the thyroid status and the level of fructose load. The inflammatory activity index averaged 5–6 points in all experimental groups. Condition I influenced the volume of infiltration by neutrophils, while dystrophic changes in hepatocytes were more dependent on the level of fructose load. Pronounced granular dystrophy of hepatocytes was revealed in all experimental groups, as well as a decrease in glycogen stores. In group II, already at a 15% fructose load, individual cells were in a state of ballooning degeneration. With a twofold increase in fructose consumption, discomplexation of hepatic plates, granular protein structures, and significant lipid accumulation in the cytoplasm of hepatocytes were observed in groups I and II. Conclusions. A high level of thyroid hormones significantly affects the indicators of inflammatory and proliferative activity of liver tissue. A low level of thyroid hormones affects the severity of dystrophic changes in hepatocytes. With an increase in fructose load, both with hypo- and hyperthyroidism, hepatocytes undergo intense dystrophic changes.
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