Switching to Regular Diet Partially Resolves Liver Fibrosis Induced by High-Fat, High-Cholesterol Diet in Mice.
Muhammad FarooqHuma HameedMarie-Thérèse Dimanche-BoitrelClaire Piquet-PellorceMichel SamsonJacques Le SeyecPublished in: Nutrients (2022)
The globally prevalent disease, non-alcoholic steatohepatitis (NASH), is characterized by a steatotic and inflammatory liver. In NASH patients, tissue repair mechanisms, activated by the presence of chronic liver damage, lead to the progressive onset of hepatic fibrosis. This scar symptom is a key prognostic risk factor for liver-related morbidity and mortality. Conflicting reports discuss the efficiency of dietary interventions on the reversibility of advanced fibrosis established during NASH. In the present study, the effect of dietary interventions was investigated in the outcome of the fibrosis settled in livers of C57BL/6J mice on a high-fat, high-cholesterol diet (HFHCD) for 5 or 12 consecutive weeks. Various clinico-pathological investigations, including a histological analysis of the liver, measurement of plasma transaminases, steatosis and fibrosis, were performed. To assess the effectiveness of the dietary intervention on established symptoms, diseased mice were returned to a standard diet (SD) for 4 or 12 weeks. This food management resulted in a drastic reduction in steatosis, liver injuries, inflammatory markers, hepatomegaly and oxidative stress and a gradual improvement in the fibrotic state of the liver tissue. In conclusion, our results demonstrated that dietary intervention can partially reverse liver fibrosis induced by HFHCD feeding.
Keyphrases
- liver fibrosis
- physical activity
- oxidative stress
- high fat diet induced
- randomized controlled trial
- weight loss
- multiple sclerosis
- insulin resistance
- systematic review
- type diabetes
- end stage renal disease
- newly diagnosed
- ejection fraction
- systemic sclerosis
- peritoneal dialysis
- wild type
- climate change
- sleep quality
- idiopathic pulmonary fibrosis
- induced apoptosis
- single molecule
- wound healing
- electronic health record
- signaling pathway