Glycerol is released from white adipose tissue as a result of lipolysis, and its flux to the liver initiates hepatic gluconeogenesis.45 In NAFLD, adipose tissue insulin resistance increases lipolysis and the glycerol flux to the liver, increasing hepatic gluconeogenesis.46 Alterations in glycerol levels and its related metabolites after FMT may thus be indicative of changes in these metabolic processes. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.