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Lab for metabolic diseases

The liver is a highly metabolically active organ that orchestrates the response to nutrient availability during fasting and feeding. Non-Alcoholic Fatty Liver Disease (NAFLD) is the most prevalent chronic liver disease worldwide. In NAFLD, hepatocytes excessively accumulate lipids, reflecting an impaired metabolic profile and response to nutrients. NAFLD can progress to Non-alcoholic steatohepatitis (NASH), where inflammation and fibrosis hamper hepatic functions and increase the risk of cirrhosis and cancer.

Our mission is to gain mechanistic insights into the etiology of NAFLD, and contribute to the development of novel therapies. We focus on the transcriptional reprogramming driven by metabolic alterations in NAFLD. We hypothesize that metabolic signalling and transcription factors cooperate to sustain disease progression and reduce therapy response. We study the microphtalmia (Mi/TFE) and nuclear receptor (NR) superfamilies at the genomic level in cell models of liver and gut, and advanced organoids.

Research interests

• modelling of metabolic diseases in organoid systems
• regulation of FXR and PPAR targets through metabolic signaling
• mechanisms of gene selectivity in hepatic TFE3 and TFEB

Key methods

• organoid generation and animal models of metabolic disease
• gene expression and genomic/transcriptomics
• bioinformatics
• conditional gene expression systems, recombinant protein production
• flow cytometry and fluorometric method development

Motivated Bachelor and Master students interested in the metabolic regulation of transcription are invited to apply for internships or thesis projects. Apply at Jose.Ramos-Pittol@uibk.ac.at .