Liver involvement dramatically worsens the prognosis in sepsis and increases mortality rates by up to 68%. The liver is essential for the regulation of pathogen-associated molecular patterns (PAMPs), including lipopolysaccharides (LPS), which are produced primarily in the gastrointestinal (GI) tract. When the integrity of the intestinal barrier is compromised in sepsis, microbial products become more permeable and move into the portal circulation, obviating hepatic clearance and triggering a destructive inflammatory cascade. The gut-liver axis, a bidirectional communication system between the gut and the liver, is primarily dependent on immunological signaling, bile acid metabolism, and the microbiome. Sepsis is often accompanied by dysbiosis, which increases intestinal permeability and impairs the synthesis of healthy metabolites such as short-chain fatty acids (SCFAs), exacerbating inflammation. On the other hand, liver failure prolongs intestinal barrier degradation by altering bile acid composition and reducing bacterial clearance. Hepatocellular injury, microcirculatory dysfunction, and systemic inflammation are all exacerbated by this vicious cycle. Restoring intestinal barrier function, modifying the microbiota, and maintaining hepatic microcirculation are therapeutic approaches that may help reduce liver damage caused by sepsis. Other strategies include targeting tight junction proteins, increasing beneficial microbial populations, neutralizing LPS using high-density lipoproteins (HDLs), and using bile acid signaling pathways such as FXR and TGR-5. The mechanisms that regulate gut-liver interactions during sepsis are not yet fully understood, despite new discoveries. To create tailored treatments that can improve the prognosis of septic patients with liver involvement, we need to expand our knowledge in this field.