Fish Oil in High-Fat Diets: A Protective Role Against Adipose Tissue Stress

A recent murine study found that fish oil in high‑fat diets preserves visceral adipose health by enhancing autophagy and reducing oxidative stress. Clinically, visceral adipose injury is a key driver of metabolic risk in obesity and may be modifiable by dietary lipid composition.

C57BL/6J mice received high‑fat diets differing only by lipid source (fish oil, lard, coconut oil, or olive oil) across obesity‑induction and intervention phases. Researchers assayed visceral adipose endpoints including LC3‑II/LC3‑I, p62, and TBARS.

The fish oil group showed a clear rise in the LC3‑II/LC3‑I ratio with a concurrent fall in p62 in visceral fat, while TBARS — a lipid peroxidation metric — were lower in fish‑oil versus lard groups. Changes were strongest in visceral depots and less marked in subcutaneous fat.

The data indicate that fish oil increased autophagic flux in visceral adipose tissue. LC3‑II/LC3‑I rose while p62 declined, consistent with greater autophagosome formation plus active lysosomal degradation. The study’s autophagy markers therefore point to productive autophagy rather than simple marker accumulation. Active autophagy in adipocytes facilitates clearance of damaged mitochondria and protein aggregates and helps maintain lipid droplet homeostasis; in this model, fish oil promoted that functional turnover instead of a stalled autophagic profile.

Regarding oxidative stress, fish oil lowered TBARS in visceral fat compared with lard, indicating reduced lipid peroxidation in the visceral depot. In contrast, lard, coconut oil and, to a lesser extent, olive oil showed marker patterns compatible with impaired autophagic flux and higher oxidative stress, aligning with greater adipose injury.