In fact, this was demonstrated earlier in a representative porcine model (given its similarity to humans) where GLP-2-induced stimulation of visceral blood flow was mediated by intestinal endocrine cells and the enteric neuron, reenforcing its clinical role in the treatment of SBS patients and making it a potential therapeutic target for low-flow gut diseases such as nonocclusive mesenteric ischemia [66]. This evidence concerns the gene GCG and macrothrombocytopenia and granulocyte inclusions with or without nephritis or sensorineural hearing loss.