Implications of gut microbiota in hepatic and pancreatic diseases: Gut-liver-pancreas axis

Table 1 Clinical and therapeutic insights-diagnostics and prognostics

Disease	Key microbiota findings in the diseased person	Therapeutic strategies using probiotics/symbiotics
Chronic hepatitis B	Reduced SCFA-producers (e.g., Roseburia, Dialister); increased Escherichia–Shigella and Proteobacteria	Restoration of microbial balance via lactobacillus and bifidobacterium strains
Liver cirrhosis	Overgrowth of Enterobacteriaceae; reduced Lachnospiraceae, Ruminococcaceae; decreased SCFA producers	Rebalancing microbiota using synbiotics; targeted probiotics
Hepatocellular crcinoma	Enrichment of Proteobacteria, Rothia; depletion of Bifidobacterium, Roseburia	Prevention in aflatoxin exposure models using probiotic mixtures
Across CLD spectrum	Gradual decrease in SCFA-producing bacteria; increased gram-negative pathogens	General microbiota modulation via diet and probiotics
Acute pancreatitis	↑ Enterococcus, ↓ Bifidobacterium in severe cases; increased IL-6 with dysbiosis	Lactobacillus plantarum reduced necrosis in RCTs; caution due to PROPATRIA trial findings
Chronic pancreatitis	↑ Proteobacteria, ↓ Firmicutes; SIBO in approximately 36% of patients	Symbiotics (e.g., Lactobacillus + FOS); PERT restores Akkermansia muciniphila
Pancreatic cancer	Oral: ↑ Porphyromonas gingivalis; Tumor: ↑ Fusobacterium, Proteobacteria	Probiotics may enhance chemotherapy; antibiotics may reduce gemcitabine-degrading bacteria
Diabetes mellitus	↓ Faecalibacterium and butyrate levels; ↑ LPS-producing taxa	SCFA supplementation; dietary prebiotics

FOS: Fructooligosaccharides; CLD: Chronic liver disease; SCFA: Short-chain fatty acids; RCT: Randomized control trials; SIBO: Small intestinal bacterial overgrowth; LPS: Lipopolysaccharide; PERT: Pancreatic enzyme replacement therapy.