Introduction: 

The present study aimed to evaluate the effect of different dietary fat sources (lard or fish oil) on cellular mechanisms involved in hepatic injury induced by chronic overfeeding. The focus was on endoplasmic reticulum (ER) stress, inflammation, apoptotic process and fibrogenesis which play important roles in the development of hepatic dysfunction.

Methods: 

Three groups of rats were fed, for 6 weeks, three different diets: standard diet (N rats), high fat diet rich in lard (40% J/J, L rats), or in fish oil (40% J/J, F rats).

Liver steatosis (by haematoxylin-eosin method) and apoptosis (by Tunel method) were assessed. eIF2a content was determined by western blot. PPARa and TGFb-1 contents were analyzed by immunocitochemistry and western blot. Mitochondrial fatty acid oxidation and oxidative stress were measured.

Results: 

F and L rats livers showed moderate diffusely mixed steatosis. PPARa content and fatty acid oxidation progressively increased in L and F rats compared to N ones. L rats showed the highest mitochondrial oxidative stress and TGFb-1 content. Apoptosis was more evident in L rats than in N and F ones. Phosphorilated eIF2a content was higher in F and L compared to N rats.

Conclusions: 

Both F and L rats showed evidence of ER stress, but high fat diet rich in fish oil, compared to high fat diet rich in lard, leads to a relatively lower grade of hepatic fat accumulation with a lower degree of oxidative stress and a lower risk to undergo to fibrosis as shown by decreased TGFb-1 production.

1.Conflict of Interest: None disclosed

2.Funding: No funding