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Liver Disease Diagnosis and Treatment · Journal article
BMC Gastroenterology · August 18, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is an exploratory randomized animal study examining whether high-intensity interval training (HIIT) combined with indole-3-propionic acid (IPA) supplementation modulates hepatic gluconeogenesis gene and protein expression in a rat model of diet-induced NAFLD. The intervention reduced gluconeogenic markers (G6Pase protein) and improved lipid and glucose parameters, but the findings are limited to surrogate endpoints in a small sample and cannot yet support human clinical practice.
Randomized controlled animal study with five parallel groups. Male Wistar rats with NAFLD induced by high-fat diet containing fructose. Intervention: 8-week high-intensity interval training (HIIT) combined with indole-3-propionic acid (IPA) supplementation. Compared with: NAFLD controls, NAFLD + HIIT alone, NAFLD + IPA alone, and non-obese controls. n = 25.
High-fat diet with fructose significantly increased lipid profile, insulin sensitivity parameters, liver enzymes (ALP, ALT, AST), G6Pase protein, and decreased FXR gene expression HIIT combined with IPA supplementation for 8 weeks resulted in significant decrease in G6Pase protein levels and increase in FXR gene expression compared to NAFLD controls Combined HIIT and IPA intervention improved lipid profile, insulin parameters, and liver enzyme levels
Surrogate molecular endpoints only; no clinical outcomes (mortality, morbidity, liver function recovery)
These findings suggest a potential mechanistic pathway by which combined exercise and IPA supplementation might improve hepatic glucose metabolism in NAFLD, but translation to human benefit remains speculative. Further controlled trials in humans are needed before clinical recommendations can be made.
Small animal study with surrogate molecular endpoints (gene expression, protein levels) and no clinical outcomes; results are mechanistically interesting but require human validation and larger controlled trials.
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These findings suggest a potential mechanistic pathway by which combined exercise and IPA supplementation might improve hepatic glucose metabolism in NAFLD, but translation to human benefit remains speculative. Further controlled trials in humans are needed before clinical recommendations can be made.
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Abstract Background Nonalcoholic fatty liver disease (NAFLD) is closely linked to metabolic disturbances such as hyperglycemia, insulin resistance, and obesity, yet the mechanisms underlying impaired hepatic gluconeogenesis remain unclear. This study addresses this gap by examining how interval training and indole-3-propionic acid (IPA) supplementation regulate the hepatic gluconeogenesis pathway in a rat model of NAFLD. Materials and methods Twenty-five male Wistar rats were randomly assigned to five groups including, control, NAFLD, NAFLD + HIIT, NAFLD + IPA, NAFLD + HIIT + IPA. At the end of the experiment, lipid profile and changes FBS and insulin and HOMA-IR as well as insulin resistance were measured in serum, changes in liver weight and liver triglyceride, as well as FXR gene expression and G6Pase protein changes in the liver tissue of all rats. Oil-red O and H&E staining were used to measure the amount of fat deposition and histopathological changes in liver tissues. Results A high-fat diet containing fructose significantly increased lipid profile, insulin sensitive parameters, as well as liver enzymes (ALP, ALT, AST) in serum, and also increased the amount of G6Pase protein and decreased FXR gene was expressed in liver tissue. However, the interaction of 8-week HIIT and IPA supplementation resulted in a significant improvement of the mentioned biomarkers, with a significant decrease in G6Pase protein levels and an increase in FXR gene expression compared to obese rats with non-alcoholic fatty liver disease. Conclusion Based on the obtained results, it seems that the interaction of HIIT and IPA supplement consumption leads to the consumption of more circulating fuels, and at the same time, it causes a decrease in gluconeogenesis and the adjustment of blood sugar and liver status, and is probably effective in preventing the complications of obesity and non-alcoholic fatty liver.
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