This research identifies molecules and mechanisms mimicking the metabolic benefits of bariatric surgery to improve adipose tissue mitochondrial energy metabolism for the treatment of obesity.

Obesity and its metabolic complications are closely linked to adipose tissue mitochondrial dysfunction. While diet-induced weight loss often fails, bariatric surgery achieves lasting metabolic improvement. After surgery, drastic increases in postprandial plasma gut hormones and bile acids are observed. However, their effects on human adipose tissue are still unknown.

This project compares patients undergoing bariatric surgery or dietary weight loss over one year, integrating clinical phenotyping with postprandial plasma metabolites, bile acids, gut hormones, and detailed mitochondrial analyses in adipose tissue. Key metabolites that are increased after bariatric surgery will be tested in human adipocyte cultures and in mouse models of obesity to identify receptors and pathways activating adipocyte mitochondrial energy metabolism for the development of novel therapeutic targets.