Thyroid Hormone Attenuate Nonalcoholic Fatty Liver Disease Via Inducing Autophagy In Rats

Background and objective: To investigate whether thyroid hormone could influence the occurrence and/or reversal of steatosis and steatohepatitis induced by a MCD diet and elucidate its molecular mechanism. Materials and Methods: Male Sprague-Dawley (SD) rats at 8 weeks of age were administered either PBS or TH intraperitoneally (0.1 g/kg per day) via stomach lavage for 6 weeks. Changes in weight gain and energy intake were regularly monitored. Blood and liver tissue were harvested after overnight fasting at the end of study. Histological assessment was performed in liver tissue. The concentrations of AST, ALT in blood and GSH, SOD and MDA in liver tissues were measured. Protein abundance involved in autophagy was analyzed in the liver. Quantification of autophagic vacuoles by transmission electron microscopy (TEM) was used to count the autophagic vacuoles. Results: After administration for 28 days, the ALT and AST content of model group rats were obvious lower compared with the control group. Results indicate that low dose chitosan can reduce hepatocellular damage and improve the liver in HF rats. TE treatment with or without exendin resulted in a similar number of autophagosomes, however, TH treatment significantly increased the number of ALs (Figure 6). While visualizing cells for AVs we observed that some large sized lipid droplets had 'shriveled' margins with distinct absence of autophagic vacuoles around them. Conclusion: The present study demonstrates that thyroid hormone might attenuate nonalcoholic fatty liver disease via inducing autophagy.