The interplay between liver health and metabolic function is increasingly understood as a complex, two-way street. New research, led by the Diabetes and Metabolic Diseases Associated (DIAMET) group at the Universitat Rovira i Virgili (URV) and the Institut d’Investigació Biomèdica de Catalunya Sud (IRB CatSud), sheds light on how liver fibrosis—scarring of the liver—disrupts hormonal balance in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease. Understanding this connection is crucial as MASLD becomes a growing public health concern, impacting millions worldwide.
MASLD, one of the most prevalent liver conditions in Western countries, encompasses a range of liver issues linked to metabolic factors like obesity, type 2 diabetes, and insulin resistance. The condition can progress from simple fat accumulation in the liver to more severe fibrosis, hindering the organ’s ability to function properly. This latest study, published in the Journal of Physiology and Biochemistry, focuses on how fibrosis and type 2 diabetes influence the body’s hormonal response, specifically after eating. Researchers found that the liver, when scarred by fibrosis, isn’t a passive bystander but actively contributes to metabolic imbalance.
The research team evaluated hormonal responses in individuals with MASLD after they consumed a standardized meal, taking into account whether they had developed liver fibrosis and/or type 2 diabetes. Their findings revealed that fibrosis is the primary driver of changes in levels of glucagon-like peptide-1 (GLP-1), a key incretin hormone responsible for regulating glucose control. Individuals with liver fibrosis exhibited higher concentrations of GLP-1 both before and after eating, regardless of their diabetes status. This suggests that even in the absence of diabetes, fibrosis significantly alters hormonal signaling.
The impact of fibrosis was even more pronounced when combined with type 2 diabetes. This combination created a synergistic effect, amplifying the hormonal alterations. Researchers emphasize that this finding reinforces the idea that a fibrotic liver isn’t simply accumulating damage, but is actively involved in disrupting hormonal regulation and contributing to metabolic imbalance. Fibrosis isn’t just a consequence of metabolic disease; it’s a factor that can exacerbate it.
The Link Between Liver Fibrosis and Hormonal Imbalance
The study’s focus on GLP-1 is significant. This incretin hormone stimulates insulin secretion and suppresses glucagon, both crucial for maintaining stable blood sugar levels. The elevated GLP-1 levels observed in individuals with fibrosis suggest the body is attempting to compensate for impaired glucose control, but the long-term effects of this sustained elevation remain unclear. Further research is needed to determine whether these elevated levels are protective or contribute to disease progression.
Implications for Diagnosis and Treatment
Given the rising prevalence of both MASLD and type 2 diabetes, understanding their hormonal interplay is critical for improving early diagnosis and optimizing treatment strategies. The research opens the door to identifying patient risk profiles based on their hormonal responses to food, paving the way for more personalized medicine. Identifying biomarkers that can predict complications or guide treatment selection is a key priority for healthcare systems. This could lead to interventions tailored to an individual’s specific hormonal profile, potentially improving outcomes.
The research was led by the Diabetes and Metabolic Diseases Associated (DIAMET) group at the URV and IRB CatSud, with collaboration from researchers at the Hospital Universitari Joan XXIII de Tarragona, the August Pi i Sunyer Biomedical Research Institute (IDIBAPS) – Hospital Clínic de Barcelona, and the Biomedical Research Centre Network (CIBER) through its areas of Diabetes and Metabolic Diseases (CIBERDEM) and Liver and Digestive Diseases (CIBEREHD).
The study, “Liver fibrosis and type 2 diabetes modulate postprandial incretin and glucagon responses in fatty liver disease,” was published in February 2026 in the Journal of Physiology and Biochemistry. You can find the full study here.
Disclaimer: This article provides information for general knowledge and informational purposes only, and does not constitute medical advice. It is essential to consult with a qualified healthcare professional for any health concerns or before making any decisions related to your health or treatment.
Researchers will continue to investigate the complex relationship between liver fibrosis, hormonal regulation, and metabolic disease. The next step will involve larger-scale studies to validate these findings and explore potential therapeutic interventions targeting the hormonal imbalances observed in MASLD. Share your thoughts and experiences with liver health in the comments below.
