Can fatty liver be a sign of a diseased gut?

Numerous liver diseases originate from prior alterations in the intestinal barrier and the gut microbiota.

The gut-liver axis has an anatomical and immunological connection that makes the liver the first organ exposed to everything that crosses the intestinal barrier.

The intestinal mucosa constitutes the body's most important biological barrier. In addition to absorbing nutrients, it acts as a defense structure capable of preventing the passage of microorganisms, endotoxins, and potentially harmful compounds into the systemic circulation.

Several factors can compromise the integrity of this barrier: coccidiosis, enterocolitis, Salmonella, dysbiosis, mycotoxins, oxidized fats, heat stress, immunosuppressive diseases, intensive vaccinations, water quality, etc.

These factors can affect the integrity of the tight junctions, which are responsible for maintaining cohesion between enterocytes and preserving barrier function.

When the intestinal barrier fails, it leads to leaky gut syndrome. This condition favors the translocation of bacteria, endotoxins (LPS), mycotoxins, and inflammatory metabolites from the intestinal lumen into the portal circulation.

All the blood from the GI tract converges in the hepatic portal vein, making the liver a true biological filter. Every molecule that crosses the barrier reaches the liver before entering the systemic circulation.

Kupffer cells, as guardians of the liver, recognize and eliminate microorganisms, endotoxins, and foreign particles from the intestine.

When activated, they release pro-inflammatory cytokines and initiate a response that often develops into chronic inflammation.

The continuous activation of these guardians generates a high production of reactive oxygen species (ROS). When free radicals exceed the body's antioxidant capacity, hepatic oxidative stress occurs. This causes hepatocellular damage and apoptosis, progressively reducing liver function.

Hepatocytes are responsible for the synthesis and export of lipid-transporting lipoproteins (Apo B100), which are essential for the formation of VLDL and LDL.
Chronic inflammation and oxidative stress disrupt Apo B100 synthesis and decrease the export of triglycerides (VLDL) from the liver, leading to hepatic steatosis and subsequent fibrosis due to stellate cell activation and loss of organ function.

In laying hens and breeders, egg production is affected, resulting in reduced egg persistence, poorer pigmentation, impaired shell quality, and hormonal and metabolic disorders.

In broilers, pigmentation and protein content are affected, leading to lower average daily gain (ADG), increased condemnations, and greater susceptibility to infectious diseases.

Therefore, liver health should be understood as an extension of gut health.

Taking care of the gut means protecting the liver.