In our study, we detected mild hepatosteatosis in all hypothyroidism-induced rats.
2
However, the composition of liver LDPs and the role of their alterations in hepatosteatosis are not well-understood.
3
In conclusion, we found that hypothyroidism-induced rats had mild hepatosteatosis as opposed to the control group histopathologically.
4
Here, we summarize recent literature reporting dissociation of hepatosteatosis from insulin resistance in genetic mouse models and clinical studies.
5
A reduction in liver fibrosis and hepatosteatosis was evident in RB394-treated obese ZSF1 rats.
6
Mitochondrial dysfunction is associated with a diverse array of diseases ranging from dystrophy and heart failure to obesity and hepatosteatosis.
7
This was accompanied by histological and gene expression analysis of adipose tissue and liver to assess adipose tissue inflammation and hepatosteatosis.
8
Thus, the ZFP36L1-dependent regulation of bile acid metabolism is an important metabolic contributor to obesity and hepatosteatosis.
9
Conclusion: PEOP extract ameliorated hepatic lipid accumulation and lipid-dependent oxidative imbalance thus showing potential applications as therapeutic agent tuning down hepatosteatosis and atherosclerosis.
10
Combined deletion of Foxo1 and Foxo3 decreased blood glucose levels, elevated serum triglyceride and cholesterol concentrations, and increased hepatic lipid secretion and caused hepatosteatosis.